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      Integrin alpha(v)beta3 promotes M21 melanoma growth in human skin by regulating tumor cell survival.

      Cancer research

      bcl-2-Associated X Protein, Animals, Antibodies, Monoclonal, pharmacology, Apoptosis, physiology, Cell Division, Cell Survival, Enzyme-Linked Immunosorbent Assay, Extracellular Matrix, metabolism, Humans, Melanoma, pathology, physiopathology, Mice, Mice, SCID, Neoplasm Proteins, antagonists & inhibitors, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-bcl-2, Receptors, Vitronectin, Skin Neoplasms, Tumor Cells, Cultured, Vitronectin

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          Abstract

          Growth and dissemination of malignant melanoma has a profound impact on our population, and little is known concerning the mechanisms controlling this disease in humans. Evidence is provided that integrin alpha(v)beta3 plays a critical role in M21 melanoma tumor survival within human skin by a mechanism independent of its known role in angiogenesis. Antagonists of alpha(v)beta3 blocked melanoma growth by inducing tumor apoptosis. Moreover, M21 melanoma cell interactions with denatured collagen, a known ligand for alpha(v)beta3, caused a 5-fold increase in the relative Bcl-2:Bax ratio, an event thought to promote cell survival. Importantly, denatured collagen colocalized with alpha(v)beta3-expressing melanoma cells in human tumor biopsies, suggesting that alpha(v)beta3 interaction with denatured collagen may play a critical role in melanoma tumor survival in vivo.

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          10363998

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