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Epigenetic regulation of gene expression significantly influences cell growth and differentiation. Here we show that epigenetic silencing of Fas determines tumor growth in vivo and apoptotic sensitivity in vitro. In established tumors with epigenetically repressed Fas, restoration of Fas activity either by transfection of fas or treatment with Trichostatin A (TSA), an inhibitor of histone deacetylase, suppresses tumor growth and restores chemosensitivity. The TSA-dependent chemosensitivity and tumor growth control require both tumor Fas and the host NK (natural killer) cell functions. This work demonstrates the importance of epigenetic modification of Fas in tumor progression and immune evasion, and emphasizes the essential interplay between Fas and innate immunity in the control of chemoresistant tumors.


Journal article


Cancer Cell

Publication Date





139 - 148


Animals, Apoptosis, Cell Differentiation, Cell Division, Cell Transformation, Neoplastic, Disease Progression, Drug Resistance, Neoplasm, Flow Cytometry, Gene Expression Regulation, Neoplastic, Histocompatibility Antigens Class I, Hydroxamic Acids, Immunity, Innate, Killer Cells, Natural, Mice, Mice, Inbred C57BL, Mice, SCID, Neoplasms, Time Factors, Transfection, Tumor Cells, Cultured, fas Receptor