J Cell Biochem

J Cell Biochem
J Cell Biochem Image link: https://en.wikipedia.org/wiki/Lithium_(medication)
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  • J Cell Biochem. 2018 May;119(5):3945-3956. doi: 10.1002/jcb.26538.(More...)
  • Bazzoni G, Hemler ME. Are changes in integrin affinity and conformation overemphasized?(More...)

POSSIBLY USEFUL

  • We test the function of procaine toward gastric cancer cells and find that procaine has the growth inhibitory and apoptosis inducement effect toward gastric cancer cells.(More...)

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KEY TOPICS

J Cell Biochem. 2018 May;119(5):3945-3956. doi: 10.1002/jcb.26538. [1] Takada Y, Murphy E, Pil P, Chen C, Ginsberg MH, Hemler ME. Molecular cloning and expression of the cDNA for alpha 3 subunit of human alpha 3 beta 1 (VLA-3), an integrin receptor for fibronectin, laminin, and collagen. J Cell Biol. 1991 Oct; 115(1):257-66. [2] J Cell Mol Med 19:1133-1150, 2015. doi: 10.1111/jcmm.12518. [3]

Huang, CY, et al. (2017) Mitochondrial ROS-induced ERK1/2 activation and HSF2-mediated AT1 R upregulation are required for doxorubicin-induced cardiotoxicity. J. Cell. [4]

Bazzoni G, Hemler ME. Are changes in integrin affinity and conformation overemphasized? Trends Biochem Sci. 1998 Jan; 23(1):30-4. [2]

POSSIBLY USEFUL

We test the function of procaine toward gastric cancer cells and find that procaine has the growth inhibitory and apoptosis inducement effect toward gastric cancer cells. [5] We report here that procaine represses the DNA-methylation level and promotes the proliferation arrest and apoptosis of gastric cancer cells. [5]

Xu Y, McDonald J, Perloff E, ButticG, Schreiber BM, Smith BD. Collagen and major histocompatibility class II expression in mesenchymal cells from CIITA hypomorphic mice. [6] Down-regulation of mitochondrial transcription factor A inhibited nuclear factor kappa-light-chain-enhancer of activated B cells (NF-?B) nuclear translocation and the expression of NF-?B depended genes. [7] From novel nuclear organization maps of human cells, they identify transcription hot zones of high gene density that are near nuclear speckles and enriched in highly expressed genes, housekeeping genes, and genes with low transcriptional pausing. [8] Intestinal organoid experiments revealed that toll-like receptor signaling in paneth cells or colonic intestinal epithelial cells induced a core set of host defense genes, but this set did not include antimicrobial peptides, which instead were induced indirectly by inflammatory cytokines. [7] Integrin signaling in carcinoma cell motility and invasion. [9] Spatial control of engulfment signaling Clearance of apoptotic cells is essential for tissue maintenance and initiated by recognition of "eat-me" ligands on the dead cells. [8] Paneth cells re-entered the cell cycle, lost their secretory expression signature, and acquired stem-like properties, thus contributing to the tissue regenerative response to inflammation. [7] The utilization of MSCs for tissue repair is initially based on the differentiation ability of these cells; however now it has been revealed that only a small fraction of the transplanted MSCs actually fuse and survive in host tissues. [10] The extracellular vesicles-derived from mesenchymal stromal cells: A new therapeutic option in regenerative medicine. - PubMed - NCBI Warning: The NCBI web site requires JavaScript to function. more. [10] The behavior of hASCs was assessed regarding cell elongation and extracellular matrix (ECM) production. [11]

Protein misfolding and aggregation lead to amyloid generation that in turn may induce cell membrane disruption and leads to cell apoptosis. [1] A significant increase in the levels of interleukin-4 (IL-4), IL-10, and transforming growth factor-?, and a decrease in the levels of IL-17 and interferon-? in concordance with the significant increase in the Treg cell ratio in splenic MNCs (P < 0.05) was shown in T1DM mice treated with AD-MSC's exosomes as compared to T1DM untreated mice. [12] In the present work, we aim to access the effect of two drugs, that is, acetylsalicylic acid and 5-amino salicylic acid on insulin amyloids by using various biophysical, imaging, cell viability assay, and computational approaches. [1] Recent findings suggest that EVs released by MSCs may also be critical in the physiological function of these cells. [10] Cell wall biosynthesis and its function in Gram-positive bacterial pathogens. [9] Cell cycle pacemaker keeps adhesion in step with division Zaidel-Bar introduces work by Jones et al. demonstrating how adhesion is regulated during the cell cycle by CDK1. [8] Aurora B kinase phosphorylation of Cdt1 influences its microtubule binding in vitro and is necessary for kinetochore-microtubule stability and mitotic progression in cells. [8]

Hurtado PA, Vora S, Sume SS, Yang D, St Hilaire C, Guo Y, Palamakumbura AH, Schreiber BM, Ravid K, Trackman PC. Lysyl oxidase propeptide inhibits smooth muscle cell signaling and proliferation. [6] Nagata Y, Jones MR, Nguyen HG, McCrann DJ, St Hilaire C, Schreiber BM, Hashimoto A, Inagaki M, Earnshaw WC, Todokoro K, Ravid K. Vascular smooth muscle cell polyploidization involves changes in chromosome passenger proteins and an endomitotic cell cycle. [6] St Hilaire C, Yang D, Schreiber BM, Ravid K. B-Myb regulates the A(2B) adenosine receptor in vascular smooth muscle cells. [6] Seidl SE, Pessolano LG, Bishop CA, Best M, Rich CB, Stone PJ, Schreiber BM. Toll-like receptor 2 activation and serum amyloid A regulate smooth muscle cell extracellular matrix. [6] Pessolano LG, Sullivan CP, Seidl SE, Rich CB, Liscum L, Stone PJ, Sipe JD, Schreiber BM. Trafficking of endogenous smooth muscle cell cholesterol: a role for serum amyloid A and interleukin-1 [6] Sullivan CP, Seidl SE, Rich CB, Raymondjean M, Schreiber BM. Secretory phospholipase A2, group IIA is a novel serum amyloid A target gene: activation of smooth muscle cell expression by an interleukin-1 receptor-independent mechanism. [6]

Both miR663a knockdown and MALAT1 activation alone significantly upregulated the expression levels of miR663a targets, including TGFB1, PIK3CD, P53, P21, and JUND, in the colon cancer cell lines HCT116 and SW480. [7] Addition of drugs at the studied concentrations attenuated the insulin fibril induced cytotoxicity in breast cancer cell line MDA-MB-231. [1]

Notch inhibition led to increased proliferation of PROX1-positive colorectal cancer cells but did not affect their ability to give rise to PROX1-negative secretory cells. [7] Isolated splenic mononuclear cells (MNCs) were subjected to splenocytes proliferation assay using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, immunophenotyping of regulatory T cells and cytokines. [12]

Human adipose-derived stem cells (hASCs) are being investigated as a promising cell source in contributing for tendon repopulation and reconstruction. [11] To gain further insights on the bi-directional crosstalk occurring between stem cells and the native tendon niche, it was used an indirect (trans-well) system for co-culturing human tendon explants and hASCs. [11]

Exosomes derived from adipose tissue-derived mesenchymal stem cells (AD-MSCs) have immunomodulatory effects of T-cell inflammatory response and reduction of clinical symptoms on streptozotocin-induced of the type-1 diabetes mellitus (T1DM). [12] Tendon explant cultures to study the communication between adipose stem cells and native tendon niche. - PubMed - NCBI Warning: The NCBI web site requires JavaScript to function. more. [11] Mesenchymal stem cells (MSCs) are adult multipotent cells that due to their ability to homing to damaged tissues and differentiate into specialized cells, are remarkable cells in the field of regenerative medicine. [10]

Irigoyen OH, Rizzolo PV, Thomas Y, Hemler ME, Shen HH, Friedman SM, Strominger JL, Chess L. Dissection of distinct human immunoregulatory T-cell subsets by a monoclonal antibody recognizing a cell surface antigen with wide tissue distribution. [2] Hemler ME, Strominger JL. Monoclonal antibodies reacting with immunogenic mycoplasma proteins present in human hematopoietic cell lines. [2] Hemler ME, Strominger JL. Characterization of antigen recognized by the monoclonal antibody (4F2): different molecular forms on human T and B lymphoblastoid cell lines. [2] Haynes BF, Hemler M, Cotner T, Mann DL, Eisenbarth GS, Strominger JL, Fauci AS. Characterization of a monoclonal antibody (5E9) that defines a human cell surface antigen of cell activation. [2] Peters PM, Kamarck ME, Hemler ME, Strominger JL, Ruddle FH. Genetic and biochemical characterization of human lymphocyte cell surface antigens. [2] Schiro JA, Chan BM, Roswit WT, Kassner PD, Pentland AP, Hemler ME, Eisen AZ, Kupper TS. Integrin alpha 2 beta 1 (VLA-2) mediates reorganization and contraction of collagen matrices by human cells. [2] Kassner PD, Hemler ME. Interchangeable alpha chain cytoplasmic domains play a positive role in control of cell adhesion mediated by VLA-4, a beta 1 integrin. [2] Weitzman JB, Pujades C, Hemler ME. Integrin alpha chain cytoplasmic tails regulate "antibody-redirected" cell adhesion, independently of ligand binding. [2] Pujades C, Alon R, Yauch RL, Masumoto A, Burkly LC, Chen C, Springer TA, Lobb RR, Hemler ME. Defining extracellular integrin alpha-chain sites that affect cell adhesion and adhesion strengthening without altering soluble ligand binding. [2] Weitzman JB, Pasqualini R, Takada Y, Hemler ME. The function and distinctive regulation of the integrin VLA-3 in cell adhesion, spreading, and homotypic cell aggregation. [2] Pasqualini R, Hemler ME. Contrasting roles for integrin beta 1 and beta 5 cytoplasmic domains in subcellular localization, cell proliferation, and cell migration. [2] Yang XH, Kovalenko OV, Kolesnikova TV, Andzelm MM, Rubinstein E, Strominger JL, Hemler ME. Contrasting effects of EWI proteins, integrins, and protein palmitoylation on cell surface CD9 organization. [2] Berditchevski F, Zutter MM, Hemler ME. Characterization of novel complexes on the cell surface between integrins and proteins with 4 transmembrane domains (TM4 proteins). [2] Yauch RL, Berditchevski F, Harler MB, Reichner J, Hemler ME. Highly stoichiometric, stable, and specific association of integrin alpha3beta1 with CD151 provides a major link to phosphatidylinositol 4-kinase, and may regulate cell migration. [2] Heino J, Ignotz RA, Hemler ME, Crouse C, MassaguJ. Regulation of cell adhesion receptors by transforming growth factor-beta. [2] Iwata J, Tung L, Urata M, Hacia J, Pelikan R, Suzuki A, Ramenzoni L, Chaudhry O, Parada C, Sanchez-Lara PA, Chai Y. Fibroblast growth factor 9 (FGF9)-pituitary homeobox 2 (PITX2) pathway mediates transforming growth factor (TGF signaling to regulate cell proliferation in palatal mesenchyme during mouse palatogenesis. [13] Koffler L, Roshong S, Park IK, Cesen-Cummings K, Thompson DC, Dwyer-Nield LC, Rice P, Mamay C, Malkinson AM, and Ruch RJ (2000) Growth inhibition in G1 and altered expression of cyclin D1 and p27kip-1 after forced connexin expression in lung and liver carcinoma cells. [14] Hanna EA, Umhauer S, Roshong SL, Piechocki MP, Fernstrom MJ, Fanning JD, and Ruch RJ (1999) Gap junctional intercellular communication and connexin43 expression in human ovarian surface epithelial cells and ovarian carcinomas in vivo and in vitro. [14]

Kiang JG, Gist ID, and Tsokos GC. Biochemical requirement of heat shock protein 72 kD expression in human breast cancer MCF-7 cells. [3] Kiang JG, Gist ID, and Tsokos GC. Cytoprotection and regulation of heat shock proteins induced by heat shock in human breast cancer T47-D cells: role of i and protein kinases. [3] Kiang JG, Gist ID, and Tsokos GC. 17?-Estradiol-induced increases in glucose-regulated proteins protect human breast cancer T47-D cells from thermal injury. [3]

Ding XZ, Smallridge RC, Galloway RJ, and Kiang JG. Increases in HSF1 translocation and synthesis in human epidermoid A-431 cells: role of protein kinase C and i. [3] Wang XD, Kiang JG, Atwa MA, and Smallridge RC. Evidence for the involvement of protein kinase C isoforms in 1 adrenergic activation of phospholipase A2 in Frtl-5 thyroid cells, J. Investig. [3]

Wang XD, Kiang JG, Scheibel LW, and Smallridge RC. Phospholipase C activation by Na+/Ca2+ exchange is essential for monensin-induced Ca2+ influx and arachidonic release in FRTL-5 thyroid cells. [3]

Ding XZ, Tsokos GC, Smallridge RC, and Kiang JG. Heat shock gene expression in HSP-70 and HSF1 gene-transfected human epidermoid A-431 cells. [3] Ding XZ, Tsokos GC, and Kiang JG. Heat shock factor 1 protein in heat shock factor 1 gene-transfected human epidermoid A-431 cells requires phosphorylation prior to inducing heat shock protein-70 production. [3] Fukumoto R, Kiang JG. Geldanamycin analog 17-DMAG limits apoptosis in human peripheral blood cells by inhibition of p53 activation and its interaction with heat shock protein 90 kDa after ionizing radiation. [3] Smallridge RC, Gist ID, Tsokos GC, and Kiang JG. Characterization of distinct heat shock and thapsigargin-induced cytoprotective proteins in FRTL-5 cells. [3] Kiang JG, Wang XD, Ding XZ, Gist I, and Smallridge RC. Heat shock inhibits the hypoxia-induced effects on iodide uptake and signal transduction and enhances cell survival in rat thyroid FRTL-5 cells. [3] Kiang JG and McClain DE. Effect of heat shock, Ca2+, and cAMP on inositol 1,4,5-trisphosphate in human epidermoid A 431 cells. [3] Kiang JG and McClain DE. N?-nitro-L-arginine decreases resting cytosolic and enhances heat stress-induced increase in cytosolic in human colon carcinoma T84 cells. [3] Kiang JG, Ding XZ, Gist ID, and Tsokos GC. Corticotropin-releasing factor increases phosphotyrosine of phospholipase C-? at tyrosine residues via its receptor 2? in human epidermoid A-431 cells. [3] Tang T, Kiang JG, Cote T, and Cox BM. Opioid-induced increase i in ND8-47 neuroblastoma X DRG hybrid cells is mediated through G protein-coupled delta opioid receptors and desensitized by chronic exposure to opioid. [3] Kiang JG, Ding XZ, and McClain DE. Thermotolerance attenuates heat-induced increases in i and HSP-72 synthesis but not heat-induced intracellular acidification in human A-431 cells. [3] Kiang JG, Ding XZ, and McClain DE. Overexpression of HSP-70 attenuates increases in i and protects human epidermoid A-431 cells after chemical hypoxia. [3] Kiang JG. Mystixin-7 and Mystixin-11 increase i and inositol trisphosphates in human A-431 cells. [3] Kiang JG, McKinney LC, and Gallin EK. Heat induces an intracellular acidification in human A 431 cells: role of Na+/H+ exchanger and metabolism. [3] Kiang JG, Wu YY, and Lin M. Hyperthermia elevates cAMP levels in human epidermoid A 431 cells. [3]

Elices MJ, Hemler ME. The human integrin VLA-2 is a collagen receptor on some cells and a collagen/laminin receptor on others. [2] Bazzoni G, Carlesso N, Griffin JD, Hemler ME. Bcr/Abl expression stimulates integrin function in hematopoietic cell lines. [2] Weitzman JB, Hemler ME, Brodt P. Reduction of tumorigenicity by alpha 3 integrin in a rhabdomyosarcoma cell line. [2] Yauch RL, Felsenfeld DP, Kraeft SK, Chen LB, Sheetz MP, Hemler ME. Mutational evidence for control of cell adhesion through integrin diffusion/clustering, independent of ligand binding. [2] Fingerman E, Hemler ME. Regulation of proteins in the VLA cell substrate adhesion family: influence of cell growth conditions on VLA-1, VLA-2, and VLA-3 expression. [2] Yang X, Claas C, Kraeft SK, Chen LB, Wang Z, Kreidberg JA, Hemler ME. Palmitoylation of tetraspanin proteins: modulation of CD151 lateral interactions, subcellular distribution, and integrin-dependent cell morphology. [2] Seipel K, Medley QG, Kedersha NL, Zhang XA, O'Brien SP, Serra-Pages C, Hemler ME, Streuli M. Trio amino-terminal guanine nucleotide exchange factor domain expression promotes actin cytoskeleton reorganization, cell migration and anchorage-independent cell growth. [2] Magda D, Lecane P, Prescott J, Thiemann P, Ma X, Dranchak PK, Toleno DM, Ramaswamy K, Siegmund KD, Hacia J. mtDNA depletion confers specific gene expression profiles in human cells grown in culture and in xenograft. [13] Comparison of alpha 4 beta 1 (VLA-4) and alpha 4 beta 7 on the human B cell line JY. J Biol Chem. 1992 Apr 25; 267(12):8366-70. [2] Nadkarni A, Rajesh C, Ruch RJ, and Pittman DL (2009) The RAD51D (E233G) genetic variant confers p53-dependent cisplatin resistance in human breast carcinoma cell lines. [14] Matesic DF, Sidorova TS, Burns TJ, Bell AM, Tran PL, Ruch RJ and May SW (2012) p38 MAPK activiation, JNK inhibition, neoplastic growth inhibition, and increased gap junction communication in human lung carcinoma and Ras-transformed cells by 4-phenyl-3-butenoic acid. [14] Fernstrom MJ, Koffler LD, Abou-Rjaily G, Boucher PD, Shewach DS, and Ruch RJ (2002) Neoplastic reversal of human ovarian carcinoma cells transfected with Connexin43. [14]

Chan BM, Matsuura N, Takada Y, Zetter BR, Hemler ME. In vitro and in vivo consequences of VLA-2 expression on rhabdomyosarcoma cells. [2] Chan BM, Elices MJ, Murphy E, Hemler ME. Adhesion to vascular cell adhesion molecule 1 and fibronectin. [2] The Hemler Lab focuses on the molecular basis for cell adhesion and migration. [2] Kolesnikova TV, Kazarov AR, Lemieux ME, Lafleur MA, Kesari S, Kung AL, Hemler ME. Glioblastoma inhibition by cell surface immunoglobulin protein EWI-2, in vitro and in vivo. [2] Hemler ME. Adhesive protein receptors on hematopoietic cells. [2] Little KD, Hemler ME, Stipp CS. Dynamic regulation of a GPCR-tetraspanin-G protein complex on intact cells: central role of CD81 in facilitating GPR56-Galpha q/11 association. [2] Heat shock protein 70 kDa plays a very important role in cell survival - a fine-line before occurrence of apoptosis. [3] They study other cell surface transmembrane proteins that associate with integrins. [2]

Stipp CS, Kolesnikova TV, Hemler ME. EWI-2 regulates alpha3beta1 integrin-dependent cell functions on laminin-5. [2] Tang W, Hemler ME. Caveolin-1 regulates matrix metalloproteinases-1 induction and CD147/EMMPRIN cell surface clustering. [2]

Kiang JG, Smith JT, Anderson MN, Swift JM, Gupta P, Balakathiresan N, Maheshwari RK. Hemorrhage exacerbates radiation effects on survival, leukocytopenia, thrombopenia, erythropenia, bone marrow cell depletion and hematopoiesis, and inflammation-associated microRNAs expression in kidney. [3] Smallridge RC, Gist ID, and Kiang JG. Na+-H+ antiport and monensin effects on cytosolic pH and iodide transport in FRTL 5 rat thyroid cells. [3] Smallridge RC, Kiang JG, Gist ID, Fein HG, and Galloway R. U 72133 inhibits TRH-induced activities in GH3 cells. [3] Aloj SM, Liguoro D, Kiang JG, and Smallridge RC. Purinergic (P2) receptor -operated calcium entry into rat thyroid cells. [3] Kiang JG, Fukumoto R. Ciprofloxacin increases survival after ionizing irradiation combined injury: gamma-H2AX formation, cytokine/chemokine, and red blood cells. [3] Kiang JG, Zhai M, Liao P-J, Bolduc DL, Elliott TB, Gorbunov NV. Pegylated G-CSF inhibits blood cell depletion, increases platelets, blocks splenomegaly, and improves survival after whole-body ionizing irradiation but not after irradiation combined with burn. [3] Gorbunov NV, Elliott TB, McDaniel DP, Lund K, Liao PJ, Zhai M, Kiang JG. Up-regulation of autophagy defense mechanisms in mouse mesenchymal stromal cells in response to ionizing irradiation followed by bacterial challenge. [3] Gorbunov NV, Elliott TB, McDaniel DP, Zhai M, Liao P-J, Kiang JG. Mitophagy and mitochondrial remodeling in mouse mesenchymal stromal cells following a challenge with Staphylococcus epidermidis. [3] Gorbunov NV, Garrison BR, McDaniel DP, Zhai M, Liao1 P-J, Nurmemet N, Kiang JG. Adaptive redox response of mesenchymal stromal cells to stimulation with lipopolysaccharide inflammagen: mechanisms of remodeling of tissue barriers in sepsis. [3] Gorbunov NV, Garrison BR, Zhai M, McDaniel DP, Ledney GD, Elliott TB, Kiang JG. Autophagy-mediated defense response of mouse mesenchymal stromal cells (MSCs) to challenge with Escherichia coli. [3] Gorbunov NV, Kiang JG. Autophagy-mediated innate defense mechanism in crypt cells responding to impairment of small intestine barrier after total-body gamma-photon irradiation. [3] Gorbunov NV, Kiang JG. Up-regulation of Autophagy in the Small Intestine Paneth Cell in Response to Total-Body ?-Irradiation. [3] Gorbunov NV and Kiang JG. Activation of IL-1? pathway and augmentation of Paneth cell ?-defensin-4 in small intestine following total-body ?-irradiation. [3]

Lin W-W, Kiang JG, and Chuang D-M. Pharmacological characterization of endothelin-stimulated phosphoinositides breakdown and cytosolic Ca2+ rise in C6 rat glioma cells. [3] Kiang JG and Koenig ML. Characterization of intracellular calcium pools in thermotolerant and their desensitization in thermotolerant cells. [3]

Peebles KA, Duncan MW, Ruch, RJ, and Malkinson AM (2003) Proteomic analysis of a mouse lung carcinoma cell line whose tumorigenicity has been abrogated by transfection with the gap junction structural gene for connexin43, Gja1. [14] Mutation and genomic deletion status of ataxia telangiectasia mutated (ATM) and p53 confer specific gene expression profiles in mantle cell lymphoma. [13] The Hacia laboratory is involved in screening of large chemical libraries for candidate small molecule therapies as well as gene therapy and cell transplantation therapy projects. [13] Nonsense suppressor therapies rescue peroxisome lipid metabolism and assembly in cells from patients with specific PEX gene mutations. [13]

Human and great ape red blood cells differ in plasmalogen levels and composition. [13] Bereiter-Hahn J, Vn M: Dynamics of mitochondria in living cells; shape changes, dislocations, fusion and fission of mitochondria. [15] Levine J, Willard M: Fodrin: Axonally transported polypeptide associated with the internal periphery of many cells. [15]

Abou-Rjaily GA, Lee SJ, May D, Al-Share QY, DeAngelis AM, Ruch RJ, Neumaier M, Kalthoff H, Lin S-H and Najjar SM (2004) CEACAM1 links metabolism to epidermal growth factor receptor-dependent cell proliferation. [14] Gentry B, Im M, Boucher PD, Ruch RJ, Shewach DS (2005) GCV phosphates are transferred between HeLa cells despite lack of bystander cytotoxicity. [14] Piechocki MP, Burk RD, and Ruch RJ (2000) Transcriptional regulation of connexin32 in rat liver cells. [14]

A possible alternative to the common VLA beta 1 subunit on certain cell lines. [2] Cells communicate with each other in many ways using secreted molecules (e.g., hormones, cytokines, growth factors, and nitric oxide), microvesicles, and direct cell contact through cellular junctions (e.g., synapses, desmosomes, hemidesmosomes, adherens junctions, and gap junctions). [14] Mechanistic differences between adhesion to CS1/fibronectin and to vascular cell adhesion molecule-1. [2] This gap junctional intercellular communication (GJIC) facilitates homeostasis, signaling and coordination of cells, and the regulation of cell birth, death and differentiation. [14] Wang N, Ingber DE: Control of cytoskeletal mechanics by extracellular matrix, cell shape and mechanical tension. [15]

TeixidJ, Hemler ME, Greenberger JS, Anklesaria P. Role of beta 1 and beta 2 integrins in the adhesion of human CD34hi stem cells to bone marrow stroma. [2] X. Qian, L. Villa-Diaz, R. Kumar, J. Lahann, and P. KrebsbachEnhancement of the propagation of human embryonic stem cells by modifications in the gel architecture of PMEDSAH polymer coatings. [16]

Kiang JG, Krishnan S, Lu X, Li Y. Inhibition of inducible nitric oxide synthase protects human T cells from hypoxia-induced injury. [3] Kiang JG, McClain DE, Warke VG, Krishnan S, and Tsokos GC. Constitutive NO synthase regulates the Na+/Ca2+ exchanger in human Jurkat T cells: role of i and tyrosine phosphorylation. [3] Krishnan S, Kiang JG, Fisher CU, Nambiar MP, Nguyen HT, Kyttaris VC, Chowdhury B, Rus V, Tsokos GC. Increased caspase-3 expression and activity contributes to reduced CD3? expression in Systemic Lupus Erythematosus T cells. [3]

Hemler ME, Brenner MB, McLean JM, Strominger JL. Antigenic stimulation regulates the level of expression of interleukin 2 receptor on human T cells. [2] Hemler ME, Jacobson JG, Brenner MB, Mann D, Strominger JL. VLA-1: a T cell surface antigen which defines a novel late stage of human T cell activation. [2] Cotner T, Hemler M, Strominger JL. Human T cell proteins recognized by rabbit heteroantisera and monoclonal antibodies. [2] Burakoff SJ, Clayberger C, Hemler M, Krensky AM, Reiss CS, Robbins E, Sanchez-Madrid F, Springer TA, Strominger JL, Ware CF. Cytotoxic T cells directed against HLA-DR antigens and their surface proteins. [2] Hemler ME, Sanchez-Madrid F, Flotte TJ, Krensky AM, Burakoff SJ, Bhan AK, Springer TA, Strominger JL. Glycoproteins of 210,000 and 130,000 m.w. on activated T cells: cell distribution and antigenic relation to components on resting cells and T cell lines. [2] Haynes BF, Mann DL, Hemler ME, Schroer JA, Shelhamer JH, Eisenbarth GS, Strominger JL, Thomas CA, Mostowski HS, Fauci AS. Characterization of a monoclonal antibody that defines an immunoregulatory T cell subset for immunoglobulin synthesis in humans. [2] Hafler DA, Hemler ME, Christenson L, Williams JM, Shapiro HM, Strom TB, Strominger JL, Weiner HL. Investigation of in vivo activated T cells in multiple sclerosis and inflammatory central nervous system diseases. [2] Hemler ME, Ware CF, Strominger JL. Characterization of a novel differentiation antigen complex recognize by a monoclonal antibody (A-1A5): unique activation-specific molecular forms on stimulated T cells. [2] Chan BM, Wong JG, Rao A, Hemler ME. T cell receptor-dependent, antigen-specific stimulation of a murine T cell clone induces a transient, VLA protein-mediated binding to extracellular matrix. [2]

Li Q, Yang XH, Xu F, Sharma C, Wang HX, Knoblich K, Rabinovitz I, Granter SR, Hemler ME. Tetraspanin CD151 plays a key role in skin squamous cell carcinoma. [2] Tachibana I, Hemler ME. Role of transmembrane 4 superfamily (TM4SF) proteins CD9 and CD81 in muscle cell fusion and myotube maintenance. [2] Lee RT, Berditchevski F, Cheng GC, Hemler ME. Integrin-mediated collagen matrix reorganization by cultured human vascular smooth muscle cells. [2] Yang XH, Flores LM, Li Q, Zhou P, Xu F, Krop IE, Hemler ME. Disruption of laminin-integrin-CD151-focal adhesion kinase axis sensitizes breast cancer cells to ErbB2 antagonists. [2] Motexafin gadolinium disrupts zinc metabolism in human cancer cell lines. [13] Kiang JG, Smith JA, and Agravante NG. Geldanamycin analog 17-DMAG inhibits iNOS and caspases in gamma irradiated human T cells. [3] I. Acquisition of a novel human cell surface protein (p80) during normal intrathymic T cell maturation. [2]

Kiang JG, Garrison BR, Smith JT, Fukumoto R. Ciprofloxacin as a potential radio-sensitizer to tumor cells and a radioprotectant for normal cells: Differential effects on ?-H2AX formation, p53 phosphorylation, Bcl-2 production, and cell death. [3] Kiang JG, Gorbunov NV. Bone marrow mesenchymal stem cells increases survival after ionizing irradiation combined with wound trauma: Characterization and therapy. [3] Kiang JG. Characterization and therapeutic uses of adult mesenchymal stem cells. [3] Kiang JG. Adult mesenchymal stem cells and radiation injury. [3]

The gene expression profiles of induced pluripotent stem cells from individuals with childhood cerebral adrenoleukodystrophy are consistent with proposed mechanisms of pathogenesis. [13]

Recent studies have focused on how certain integrins may be linked to regulation of matrix metalloproteinase (MMP) production, a key process during cell and tissue remodeling and tumor cell metastasis. [2] Cell adhesion is a basic process in cell biology, controlling cell growth, death, differentiation, movement, and tissue organization in normal cells, as well as the proliferation and metastasis of tumor cells. [2]

Ghosh, P.M., Bedolla, R., Thomas, C.A. and Kreisberg, JI. Role of Protein kinase C in Arginine Vasopressin-stimulated mesangial cell proliferation. [17] Yang J, Craddock L, Hong S, Liu ZM. AMP-activated protein kinase suppresses LXR dependent sterol regulatory element-binding protein-1c transcription in rat hepatoma McA-RH7777 cells. [18] Zhang JM, Murakumo Y, Hagiwara S, Jiang P, Mii S, Kalyoncu E, Saito S, Suzuki C, Sakurai Y, Numata Y, et al. CD109 attenuates TGF-beta1 signaling and enhances EGF signaling in SK-MG-1 human glioblastoma cells. [19] Shiraki Y, Mii S, Enomoto A, Momota H, Han YP, Kato T, Ushida K, Kato A, Asai N, Murakumo Y, et al. Significance of perivascular tumour cells defined by CD109 expression in progression of glioma. [19] Litvinov IV, Bizet AA, Binamer Y, Jones DA, Sasseville D, Philip A. CD109 release from the cell surface in human keratinocytes regulates TGF-beta receptor expression, TGF-beta signalling and STAT3 activation: relevance to psoriasis. [19] On the cell surface, CD109 negatively regulates the TGF-?1 signaling pathway via formation of a receptor complex with TGF-?R1 and TGF-?R2 in human keratinocytes. [19] Although knockdown of CD109 in human keratinocytes and lung adenocarcinoma cells downregulates STAT3 signaling in vitro, the CD109-deficient mice displayed opposite results. [19] They also investigated CD109 expression in five human cervical carcinoma cell lines, and observed high levels of CD109 expression in two SCC cell lines. [19] Hagiwara et al. demonstrated that oral SCC cell lines overexpression CD109 accelerated cell proliferation and impaired the anti-proliferative effect mediated by TGF-?1. [19] The membrane-anchored CD109 in SK-MG-1 cells directly interacts with EGFR and enhances EGF signaling, which subsequently increases cell migration and invasion, while the secreted CD109 has no effect on EGF signaling. [19] CD109 may exert distinct regulatory effects in different cell types, leading to cell-type specific modification in STAT3 signaling. [19] A high level of CD109 expression inhibited Smad2 phosphorylation, thus attenuated TGF-?1/Smad2 signaling and impairs TGF-?1-mediated suppression of cell growth, CD109 knockdown increased Smad2 phosphorylation by TGF-?1 stimulation. [19] In the normal lung tissues, CD109 expression was confined mainly to basal cells of the bronchial and bronchiolar epithelia. [19] In the non-diseased esophageal tissue, CD109 expression was restricted in cytosol of the stratified epithelial cells at a weak level. [19] Besides, Chuang et al. reported that CD109 expression was dramatic upregulated in metastatic lung adenocarcinoma cells, and cells expressing a CD109 shRNA (shCD109) showed a dramatic reduction in STAT3 phosphorylation. [19]

Dong F, Cheng Y, Sun Q, Lu W, Zhang G, Li L, Allen TD, Liu J. CD109 is specifically expressed in endothelial cells of cutaneous cavernous haemangioma. [19] Li W, Liu J, Zhao Y. PKM2 inhibitor shikonin suppresses TPA-induced mitochondrial malfunction and proliferation of skin epidermal JB6 cells. [20] Shi Y, Massague J. Mechanisms of TGF-beta signaling from cell membrane to the nucleus. [19] Lakhter AJ, Hamilton J, Dagher PC, Mukkamala S, Hato T, Dong XC, et al. Ferroxitosis: a cell death from modulation of oxidative phosphorylation and PKM2-dependent glycolysis in melanoma. [20]

Human PKM1 (#44241) and PKM2 (#44242) in pET28a vector were purchased from addgene expressed as an N-terminal His 6 tag fusion protein. pET28a-PKM1 and pET28a-PKM2 was transformed into BL2 (DE3) pLysS cells and grown to an absorbance of 0.8 at 600 nm, then induced with 0.5 mM IPTG for 7 h at room temperature. [20] The N-terminal leader peptide anchor the protein to the inner membrane within the periplasm and the N-terminal fragment of CD109 secreted from cells after cleavage by the furin protease. [19] Lin M, Sutherland DR, Horsfall W, Totty N, Yeo E, Nayar R, Wu XF, Schuh AC. Cell surface antigen CD109 is a novel member of the alpha(2) macroglobulin/C3, C4, C5 family of thioester-containing proteins. [19] Cell surface antigen CD109 is a glycosylphosphatidylinositol (GPI)-linked glycoprotein of approximately 170 kDa and a member of the a2 macroglobulin (a2M)/C3, C4, C5 family of thioester-containing proteins. [19]

CD109 can be released from the cell surface by cellular lipases such as phosphatidylinositol-specific phospholipase C (PI-PLC). [19] In vitro, they found that transfection of CD109 siRNA down-regulates STAT3, release of CD109 from the cell surface of cultured human keratinocytes. [19] Litvinov et al. found that CD109 released from the cell surface into the extracellular milieu, and the released form of CD109 retains its ability to induce intracellular signaling pathways. [19] Loss of CD109 in all the cells in mice might modify the subcutaneous microenvironment which activates STAT3 signaling in keratinocytes. [19] To date the relationship of CD109 and STAT3 signaling have not been explored in these cell types. [19] CD109 interact with JAK/STAT3 and EGFR signaling pathways in other cell types. [19] OSCC cell lines overexpressing CD109 exhibited accelerated cell growth in vitro, implicating that CD109 involves in the progression of OSCCs. [19] CD109 was first identified as a cell-surface antigen by a monoclonal antibody raised against the primitive lymphoid/myeloid cell line KG1a. [19] In the normal skins, CD109 was weakly expressed in the basal layer of epidermal cells, while strands of malignant squamous epidermal cells displayed strong CD109 staining. [19] In all the ESCC samples from the TMAs, strands of malignant squamous epithelial cells displayed strong CD109 staining in the cytosol. [19] In addition to keratinocytes, CD109 is expressed in endothelial cells, epithelial cells, and fibroblasts, which participate in constitute the skin tissue. [19] Inhibition of JAK kinase activity in fibroblasts overexpressing CD109 reduced phosphorylated STAT3 to a level similar to that in the parental cells expressing low levels of CD109, suggesting that CD109-induced STAT3 phosphorylation requires JAK kinase activity. [19] Pyruvate kinase activity in cell extracts of the melanoma cell line MEL103 pretreated with different concentrations of lapachol (0 ?M, 10 ?M, 20 ?M and 40 ?M) for 24 hours and the enzyme activity was assessed using Pyruvate Kinase Activity (Bio Vision, K709-100). [20] Each value represents mean ECAR value se from five replicates (B) Oxygen consumption rate (OCR) under basal and maximal (after the addition of FCCP 30 ?M) were plotted for MEL 526 and MEL103 cell lines after the treatment of cell lines with lapachol at concentrations 0 ?M, 5 ?M, 10 ?M, 20 ?M and 40 ?M overnight. [20] Lapachol (20 ?M) treatment increased annexin positive cells to 13% but the combined treatment of lapachol (20 ?M) and DNP (10 ?M) further increased the percentage of annexin positive cells to 20%. (B) Loss of mitochondrial membrane potential was analyzed by TMRM dye in MEL 103 melanoma cell line after treatment with DMSO (Vehicle), lapachol (20 ?M), DNP (10 ?M) and lapachol (20 ?M) +DNP (10 ?M). [20]

Lapachol showed a dose-dependent decrease in extra cellular acidification rate (ECAR) in both MEL526 and MEL103 cells ( Fig 2A ). [20] In normal mice, TXNIP deficiency induced metabolic aging of mice and cellular senescence of kidney cells by inducing AKT activity and aging-associated gene expression. [21] Interestingly, TXNIP MEF cells showed continuous activation of AKT during long-term subculture, and AKT signaling inhibition completely blocked the cellular senescence of TXNIP MEF cells. [21] The TGF-? signaling pathway is involved in many cellular processes including cell growth, cell differentiation apoptosis, and cellular homeostasis. [19] Chen, Q, et al. (2016) FGF-2 Transcriptionally Down-Regulates the Expression of BNIP3L via PI3K/Akt/FoxO3a Signaling and Inhibits Necrosis and Mitochondrial Dysfunction Induced by High Concentrations of Hydrogen Peroxide in H9c2 Cells. [4] As the mechanism of action of high glucose is unknown, we undertook the investigation of the signaling pathway on the upregulation of Txnip expression induced by high glucose in rat mesangial cells. [21] High glucose condition upregulated Txnip expression level in rat mesangial cells through ROS/MEK/MAPK pathway. [21]

Yeh, Y, et al. (2016) Hypoxia Augments Increased HIF-1 and Reduced Survival Protein p-Akt in Gelsolin (GSN)-Dependent Cardiomyoblast Cell Apoptosis. [4] Vascular endothelial cells senescence is associated with NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation via reactive oxygen species (ROS)/thioredoxin-interacting protein (TXNIP) pathway. [21] Cytoscription: Computer-controlled micropositioning of cell adhesion proteins. [17] Thioredoxin-interacting protein mediates high glucose-induced reactive oxygen species generation by mitochondria and the NADPH oxidase, Nox4, in mesangial cells. [21]

Quan, K, et al. (2017) Icariside II induces cell cycle arrest and apoptosis in human glioblastoma cells through suppressing Akt activation and potentiating FOXO3a activity. [4] Phosphorylated R-SMADs then form heteromeric complexes with Smad4, combined with transcription factors, regulate gene transcription and cell function. [19] Time lapse images were obtained with a custom spinning-disk microscope built around a CSU-10 Confocal head (Yokogawa), a 897 Xion EMCCD camera (Andor), a 4-line monolithic laser launch (Agilent) and a TiE inverted microscope stand (Nikon) equipped with a stage top incubator that regulates CO2 at 5% and temperature at 37C. The cells were imaged at an interval of 3 minutes for a total period of 3 hours. [20]

Kent MS, Zwingenberger A, Westropp JL, Barrett LE, Durbin-Johnson BP, Ghosh P, Vinall RL. MicroRNA profiling of dogs with transitional cell carcinoma of the bladder using blood and urine samples. [17] The anti-cancer activity of lapachol when tested against leukemia, sarcoma and Walker 256 carcinoma cells showed that only Walker 256 carcinoma cells were sensitive to this compound. [20] The effects of lapachol on glycolytic capacity were prominent as high concentrations of lapachol completely blunted glycolytic capacity in melanoma cells. [20] The differential effects of lapachol on ATP levels in these cells could be attributed to differences in oncogenic background, as MEL526 is a BRAF mutant and MEL103 harbors an NRAS mutation. [20] To evaluate the cytotoxic effects of naphthoquinones, MEL526, MEL103 and MEL697 cells under hypoxia were treated with menadione (20 uM), shikonin (5, 10 and 20uM) or lapachol (5, 10 and 20uM), and cell viability was determined ( Fig 1B ). [20] Because lapachol is an analog of shikonin ( Fig 1A ), we tested the biological effects of this compound on cells under hypoxia. [20] An important clue for assessing the effects of lapachol on pigment producing melanoma cells came from a zebrafish study. [20] Vander Heiden MG, Cantley LC, Thompson CB. Understanding the Warburg effect: the metabolic requirements of cell proliferation. [20] Blockade of glycolysis by lapachol in melanoma cells led to decreased ATP levels and inhibition of cell proliferation. [20] Lapachol inhibit PKM2 activity and reduces ATP levels to inhibit cell proliferation. [20] MEL526 and MEL103 cells were exposed to various concentrations of lapachol and cell number was quantified to determine cell proliferation. [20] High concentrations of lapachol (20-40 uM) significantly inhibited the rate of proliferation in both MEL526 and MEL103 cells. [20] As much as 10 uM lapachol was sufficient to reduce cell proliferation to half of control cells ( Fig 5A ). [20] Our data show that both BRAF and NRAS mutant melanoma cell proliferation is reduced by lapachol. [20] Melanoma cells treated with lapachol showed a dose-dependent inhibition of glycolysis and a corresponding increase in oxygen consumption. [20] To assess if this inhibition of glycolysis increases oxygen consumption, melanoma cells were treated with different concentrations of lapachol and oxygen consumption rate (OCR) was recorded. [20] Consistent with a decrease in lapachol-mediated ECAR, a dose-dependent increase in OCR was observed in cells exposed to lapachol ( Fig 2B ). [20] Although MEL103 cells exposed to lapachol or DNP showed about 10% apoptotic cells, lapachol combined with DNP showed a 20% increase in apoptosis ( Fig 6A ). [20] To test if inhibition of glycolysis with lapachol sensitizes melanoma cells to the mitochondrial drug dinitrophenol (DNP), MEL103 cells were treated with lapachol or DNP or a combination of lapachol and DNP for overnight and apoptosis was assessed by flow cytometry. [20] Because PKM2 is expressed in fetal tissues and in malignant cells, we hypothesized that lapachol may target PKM2. [20] We report that unlike its structural analog shikonin, a known inhibitor of PKM2, lapachol failed to induce non-apoptotic cell death ferroxitosis in hypoxia. [20] Lapachol inhibited PKM2 activity of purified enzyme as well as in melanoma cell extracts. [20] Lapachol inhibited PKM2 activity in the cell extracts in a dose dependent manner ( Fig 4C ). [20] Here we present biochemical, metabolic and computational modeling evidence suggesting that lapachol targets PKM2 in inhibition of glycolysis, and sensitizes melanoma cells to apoptosis. [20] To further validate these results, MEL103 cells were exposed to various concentration of lapachol and the enzyme activity of PKM2 was determined in the cell extracts. [20] To test this possibility, lapachol treated MEL526 and MEL103 cells were subjected to Seahorse analysis. [20] Although MEL526 cells showed a dose-dependent decrease in ATP levels, 10 uM lapachol inhibited 50% of ATP levels in MEL103 cells ( Fig 5B ). [20] MEL103 cells exposed to lapachol or DNP maintained TMRM fluorescence suggesting mitochondrial integrity, whereas the combination of these drugs led to loss of mitochondrial membrane potential ( Fig 6B ). [20] MEL103 cells were exposed to lapachol or DNP or combination of these drugs for 12 hours and treated with TMRM prior to live-cell imaging ( S1 - S4 Videos). [20] Mitochondrial membrane integrity in vehicle, lapachol (20 ?M) and DNP (10 ?M) treated cells and loss of mitochondrial membrane potential is revealed in cells treated with a combination of lapachol (20 ?M) and DNP (10 ?M) as reflected by the loss of TMRM fluorescence intensity. [20] NRAS mutant MEL103 cells treated with lapachol were sensitive to DNP in promoting apoptosis. [20] Perturbation of glycolysis in melanoma cells with lapachol sensitized cells to mitochondrial protonophore and promoted apoptosis. [20] Lapachol showed a moderate decrease in cell viability at high concentrations. [20] Lapachol is an effective inhibitor of glycolysis in melanoma cells. [20] Cell viability determination in normoxia also revealed that unlike menadione, lapachol was not cytotoxic to cells ( S1 Fig ). [20] These results establish that lapachol inhibits glycolysis as a result of it, cells switch to oxidative phosphorylation for cell survival. [20] Based on our results that lapachol inhibits glycolysis in melanoma cells, we hypothesized that lapachol interacts with the key glycolysis regulator, PKM2. [20] Our results showed that lapachol was not cytotoxic to melanoma cells, yet it inhibited PKM2 activity and glycolysis. [20] Luo W, Semenza GL. Emerging roles of PKM2 in cell metabolism and cancer progression. [20] Now, Chen and his team are dissecting a signaling pathway involving a novel DNA sensor - cyclic GMP-AMP (cGAMP) synthase, or cGAS - which activates an interferon response that may play a role in immune defense against pathogens and malignant cells, as well as in autoimmune diseases such as lupus. [22] They found that TGF-? signaling inhibits endothelial cell proliferation and migration, while TGF-? signaling also induces these processes via ALK1-Smad1/5. [19] Chang, YM, et al. (2017) Alpinia oxyphylla Miq. fruit extract activates IGFR-PI3K/Akt signaling to induce Schwann cell proliferation and sciatic nerve regeneration. [4] Signal transducer and activator of transcription factor 3 (STAT3) is critical to cell proliferation, differentiation, migration, survival, and oncogenesis. [19] The activation of EGFR promotes cell migration, survival, and proliferation. [19]

Despite these findings of metabolic reprograming in malignant cells, lack of pharmacological tools that specifically target aerobic glycolysis has limited our efforts in exploiting critical metabolic vulnerabilities towards devising effective cancer treatment strategies. [20] No CD109 positive staining was observed in other cell types. [19] As CD109 is distinctly expressed in malignant sqamous cells in gallbladder, CD109 may be a diagnostic marker for gallbladder SCCs and ASCs. [19] CD109 positive cells were found in 86.7% of SCCs and 91.7% of ASCs. [19] SCC cells with CD109 knockdown exhibited slower cell growth. [19] Exogenous CD109 has been identified as a component of exosome secreted from transfected 293 cells, making it a promising target for exosome diagnosis. [19]

Narayanan, K.N., Ali, M., Barclay, B., Cheng, Q.S., D'Abronzo, L.S., Dornetshuber-Fleiss, R., Ghosh, P.M., et al, Disruptive environmental chemicals and cellular mechanisms that confer resistance to cell death. [17] TXNIP MEF cells showed greater induced glucose uptake and ROS levels than wild-type cells, and N-acetylcysteine (NAC) treatment rescued the cellular senescence of TXNIP MEF cells. [21]

Effect of cyclin E overexpression on lovastatin-induced G1 arrest and RhoA inactivation in NIH3T3 cells. [17] This study explores the effects and possible mechanisms of NLRP3 inflammasome in endothelial cells senescence. [21]

Liao, PH, et al. (2017) Phosphorylation of cofilin-1 by ERK confers HDAC inhibitor resistance in hepatocellular carcinoma cells via decreased ROS-mediated mitochondria injury. [4] MEL526, and MEL697 melanoma cell lines were maintained in RPMI1640 (HyClone) medium and MEL103 and A375 cell lines were maintained in DMEM (Life Technologies), supplemented with 10% fetal bovine serum (Sigma), 50 units ml ?1 penicillin and 50 ?g ml ?1 streptomycin (Life Technologies). [20] As we reported, menadione failed to promote cell death in hypoxia and shikonin induced ferroxitosis in a dose-dependent manner in all the cell lines tested. [20]

Electrical Measurements can be used to Monitor the Attachment and Spreading of Cells in Tissue Culture. [17] Aging is associated with an inevitable and universal loss of cell homeostasis and restricts an organism's lifespan by an increased susceptibility to diseases and tissue degeneration. [21]

The assay for PKM activity determination contained recombinant pyruvate kinase (100 ng) or cell lysate (5?g), Tris pH 7.5 (50 mM), KCl (100 mM), ADP (0.6 mM), PEP (0.5 mM), NADH (180?M) and LDH (8 units). [20] Xu J, Chu T, Jin B, Dong X, Lou Y, Zhang X, Wang H, Zhong H, Shi C, Gu A, et al. Epidermal growth factor receptor tyrosine kinase inhibitors in advanced squamous cell lung cancer. [19] Sato T, Murakumo Y, Hagiwara S, Jijiwa M, Suzuki C, Yatabe Y, Takahashi M. High-level expression of CD109 is frequently detected in lung squamous cell carcinomas. [19] Zhang JM, Hashimoto M, Kawai K, Murakumo Y, Sato T, Ichihara M, Nakamura S, Takahashi M. CD109 expression in squamous cell carcinoma of the uterine cervix. [19] Megumi K, Ishigami S, Uchikado Y, Kita Y, Okumura H, Matsumoto M, Uenosono Y, Arigami T, Kijima Y, Kitazono M, et al. Clinicopathological significance of BMP7 expression in esophageal squamous cell carcinoma. [19] Hanawa M, Suzuki S, Dobashi Y, Yamane T, Kono K, Enomoto N, Ooi A. EGFR protein overexpression and gene amplification in squamous cell carcinomas of the esophagus. [19] Shinagawa K, Yanamoto S, Naruse T, Kawakita A, Morishita K, Sakamoto Y, Rokutanda S, Umeda M. Clinical roles of interleukin-6 and STAT3 in oral squamous cell carcinoma. [19]

Joshi A, Zanwar S, Noronha V, Patil VM, Chougule A, Kumar R, Janu A, Mahajan A, Kapoor A, Prabhash K. EGFR mutation in squamous cell carcinoma of the lung: does it carry the same connotation as in adenocarcinomas? Onco Targets Ther. 2017;10:1859-63. [19] Jedlinski A, Garvin S, Johansson AC, Edqvist PH, Ponten F, Roberg K. Cetuximab sensitivity of head and neck squamous cell carcinoma xenografts is associated with treatment-induced reduction in EGFR, pEGFR, and pSrc. [19] Dong F, Liu F, Yan S, Liu X, Jiang Z, Liu J. Elevated expression of CD109 in esophageal squamous cell carcinoma. [19] Dong F, Wang Y, Li L, Wang Y, Liu X, Liu J. CD109 expression is increased in cutaneous squamous cell carcinoma. [19] Dong F, Wang J, Xu Y, Cheng Z, Chen X, Wang Y, Liu J. CD109 expression is upregulated in penile squamous cell carcinoma. [19]

Chen B, Li C, Zhang L, Lv J, Tong Y. Screening of biomarkers in cervical squamous cell carcinomas via gene expression profiling. [19] He Y, Liu J, Zhao Z, Zhao H. Bioinformatics analysis of gene expression profiles of esophageal squamous cell carcinoma. [19]

CD109 expression was examined in human lung cell carcinomas by quantitative RT-PCR, which showed a significantly higher expression of CD109 in squamous cell carcinomas, but not in adenocarcinomas, large-cell carcinomas or small-cell carcinomas. [19] Studies from human tissue samples indicate that CD109 is highly expressed in SCCs of multiple organs, particularly in well-differentiated malignant squamous cells. [19] Dong et al. demonstrated that CD109 protein is highly expressed in malignant squamous cells of PSCCs compared with normal penile tissues on TMAs. [19] Subtypes of GBCs tissues including adenocarcinoma (AC), squamous cell carcinoma (SCC), and adenosquamous carcinoma (ASC) were examined on TMAs by immunohistochemical staining with a CD109 antibody. [19] Gonzales CB, De La Chapa JJ, Saikumar P, Singha PK, Dybdal-Hargreaves NF, Chavez J, Horning AM, Parra J, Kirma NB. Co-targeting ALK and EGFR parallel signaling in oral squamous cell carcinoma. [19] Languino LR, Singh A, Prisco M, Inman GJ, Luginbuhl A, Curry JM, South AP. Exosome-mediated transfer from the tumor microenvironment increases TGFbeta signaling in squamous cell carcinoma. [19] Osawa H, Nakajima M, Kato H, Fukuchi M, Kuwano H. Prognostic value of the expression of Smad6 and Smad7, as inhibitory Smads of the TGF-beta superfamily, in esophageal squamous cell carcinoma. [19] Previous studies have shown that the high expression of CD109 in SCCs and the limited expression in normal squamous cells (Table 1 ). [19] Squamous cell carcinoma (SCC) is one of the most common cancers of epithelial origin. [19] Lung squamous cell carcinoma (LSCC) is one of the major subtypes of non-small-cell lung cancer (NSCLC), and accounts for approximately 20-30% of cases of NSCLCs. [19] Cutaneous squamous cell carcinoma (CSCC) is the second most common type of non-melanoma skin cancer (NMSC) with a constantly increasing incidence. [19] Oral squamous cell carcinoma (OSCC) accounts for 2-3% of all cancers worldwide. [19] Nie XJ, Liu WM, Zhang L. Association of VEGF gene polymorphisms with the risk and prognosis of cutaneous squamous cell carcinoma. [19] Stoner GD, Wang LS, Chen T. Chemoprevention of esophageal squamous cell carcinoma. [19] Nazir SA, Heetun M, Walsh JL, Lole Harris BH. Hello, is it SCC you are looking for? Squamous cell carcinoma of the penis presenting as an inguinal mass. [19] Squamous cell carcinoma (SCC) is well-known for its high rate of metastasis with poor prognosis. [19] Penile squamous cell carcinoma (PSCC) is a subtype of CSCCs and has rarely been studied. [19] Gallbladder squamous cell carcinoma (GSCC) accounts 3% of the malignant neoplasm of this organ. [19] Thompson LD. Laryngeal dysplasia, squamous cell carcinoma, and variants. [19] Wesola M, Jelen M. Morphometric differentiation of squamous cell carcinoma and adenocarcinoma of the cervix. [19] Connolly EC, Akhurst RJ. The complexities of TGF-beta action during mammary and squamous cell carcinogenesis. [19]

Li W, Liu J, Jackson K, Shi R, Zhao Y. Sensitizing the therapeutic efficacy of taxol with shikonin in human breast cancer cells. [20] Haq R, Shoag J, Andreu-Perez P, Yokoyama S, Edelman H, Rowe GC, et al. Oncogenic BRAF regulates oxidative metabolism via PGC1alpha and MITF. Cancer cell. 2013;23(3):302-15. [20] Citation: Shankar Babu M, Mahanta S, Lakhter AJ, Hato T, Paul S, Naidu SR (2018) Lapachol inhibits glycolysis in cancer cells by targeting pyruvate kinase M2. [20] Ghosh-Choudhury, N., Ghosh-Choudhury, G., Celeste, A., Ghosh, P.M., Moyer, M.L., Abboud, S.L., and Kreisberg, J.I. Bone Morphogenic Protein-2 induces cyclin kinase inhibitor p21 and hypophosphorylation of retinoblastoma protein in estradiol treated MCF- human breast cancer cells. [17] Hsu, HH, et al. (2016) Taiwanin E inhibits cell migration in human LoVo colon cancer cells by suppressing MMP-2/9 expression via p38 MAPK pathway. [4] Chen, L, Lu, X. -H., Shi, X. -B., R., deVere White, RW, Carraway, K.L. III and Ghosh, PM. Nrdp1-mediated regulation of ErbB3 expression by the androgen receptor in androgen-dependent but not castrate-resistant prostate cancer cells. [17] Chen J, Xie J, Jiang Z, Wang B, Wang Y, Hu X. Shikonin and its analogs inhibit cancer cell glycolysis by targeting tumor pyruvate kinase-M2. [20] Ning X, Qi H, Li R, Li Y, Jin Y, McNutt MA, et al. Discovery of novel naphthoquinone derivatives as inhibitors of the tumor cell specific M2 isoform of pyruvate kinase. [20] Chen H, Libertini SJ, Wang Y, Kung HJ, Ghosh P, Mudryj M. ERK regulates calpain 2-induced androgen receptor proteolysis in CWR22 relapsed prostate tumor cell lines. [17] Previous studies reported that CD109 is expressed on a subset of fetal and adult CD34 + positive bone marrow mononuclear cells, activated T lymphoblasts, activated platelets, endothelial cells, mesenchymal stem cell subsets and several human tumor cell lines, but not expressed in resting human T cells, platelets or peripheral blood leukocytes. [19] Shiraki et al. reported CD109-positive perivascular tumor cells in human lower-grade glioma tissues and in a mouse model recapitulated human glioma, suggesting a key role of CD109 for this disease. [19] To date CD109 have not been reported in exosomes derived from SCC or other tumor cells. [19]

Giesert C, Marxer A, Sutherland DR, Schuh AC, Kanz L, Buhring HJ. Antibody W7C5 defines a CD109 epitope expressed on CD34+ and CD34? hematopoietic and mesenchymal stem cell subsets. [19] Deshmukh A, Deshpande K, Arfuso F, Newsholme P, Dharmarajan A. Cancer stem cell metabolism: a potential target for cancer therapy. [20] Our findings that glycolysis inhibition by lapachol sensitized tumor cells to the mitochondrial drug DNP demonstrate that a combination of agents that target both tumor cell glycolysis and mitochondrial metabolism may be an effective strategy to treat cancer. [20] Therefore, lapachol is a novel natural product and can be used as a tool to target tumor cell glycolysis and better understand cancer metabolism. [20] The activity of BRAF inhibitors on tumor cell metabolism is reminiscent of the effects of lapachol. [20] Our data reveal lapachol as an inhibitor of glycolysis, which is critical for tumor cell proliferation. [20] These results present lapachol as an inhibitor of PKM2 to interrogate metabolic plasticity in tumor cells. [20] We hypothesized that lapachol inhibits tumor cell glycolysis in exerting anti-cancer activity. [20]

Mazurek S. Pyruvate kinase type M2: a key regulator of the metabolic budget system in tumor cells. [20] Although pyruvate kinase M2 (PKM2) is a key mediator of glycolysis in cancer cells, lack of selective agents that target PKM2 remains a challenge in exploiting metabolic pathways for cancer therapy. [20] Chen, H., Libertini, S.J., George, M., Dandekar, S., Tepper, C.G., Al-Bataina, B., Kung, H. -J., Ghosh, P.M., Mudryj, M. Genome-wide analysis of androgen receptor binding and gene regulation in two CWR22-derived prostate cancer cell lines. [17] Mooso, B., Madhav, A. Johnson, S.D., Roy, M., Moore, M.E., Moy, C., Loredo, Mehta, R.G., Vaughan, A.T.M. and Ghosh, P.M. Androgen Receptor regulation of Vitamin D receptor in response of castration-resistant prostate cancer cells to 1?-Hydroxyvitamin D5 - a calcitriol analog. [17] Wang, Y., Kreisberg, J.I., Bedolla, R., Mikhailova, M., deVere White, R.W. and Ghosh, P.M. A 90 kDa fragment of filamin A promotes Casodex-induced growth inhibition in Casodex-resistant androgen receptor positive C4-2 prostate cancer cells. [17] Chen L, Mooso BA, Jathal MK, Madhav A, Johnson SD, van Spyk E, Mikhailova M, Zierenberg-Ripoll A, Xue L, Vinall RL, deVere White RW, Ghosh PM. Dual EGFR/HER2 inhibition sensitizes prostate cancer cells to androgen withdrawal by suppressing ErbB3. [17] Role of RhoA and actin stress fiber formation in the proliferation of a mouse prostate cancer cell line. [17] Because aerobic glycolysis is characteristic of cancer cells, lapachol can be used to block glycolysis regardless of the oncogenic mutations. [20] This lactate production partly explains the reason for subdued mitochondrial functions in cancer cells, as mitochondrion is a suitable location for NAD regeneration. [20]

Tumor cells metabolize glucose even in the presence of oxygen by a process commonly referred to as aerobic glycolysis or the Warburg effect. [20] Although normal cells express the PKM1 isoform, fetal tissues and tumor cells predominantly express the PKM2 isoform, which is enzymatically less active than PKM1. [20]

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2. (68) Lapachol inhibits glycolysis in cancer cells by targeting pyruvate kinase M2

3. (53) Martin E. Hemler, PhD - Dana-Farber Cancer Institute | Boston, MA

4. (45) Uniformed Services University

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6. (11) Randall J. Ruch, Ph.D.

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8. (8) Joseph Hacia | USC Profiles

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10. (7) Barbara M. Schreiber | Biochemistry

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19. (2) Core Faculty | Molecular & Cellular Biochemistry

20. (1) Xu Qian | School of Dental Medicine

21. (1) Craddock, MD, Lauren Department of Dermatology UW-Madison

22. (1) Zhijian "James" Chen, PhD | HHMI.org

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