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• W2897735072 abstract "Expression of the class II a HDAC s is frequently altered in different human cancers. In mouse models these transcriptional repressors can trigger transformation, acting as bona fide oncogenes. Whether class II a HDAC s also exhibit transforming activities in human cells is currently unknown. We infected primary human fibroblasts with retroviruses to investigate the transforming activity of HDAC 4 in cooperation with well‐known oncogenes. We have discovered that HDAC4 triple mutant (S246A, S467A, S632A) (HDAC4‐ TM) , a nuclear resident version of the deacetylase, triggers TP 53 stabilization and OIS (oncogene‐induced senescence). Unlike RAS , HDAC 4‐induced OIS was TP 53‐dependent and characterized by rapid cell cycle arrest and accumulation of an unusual pattern of γH2 AX ‐positive foci. The inactivation of both TP 53 and of the retinoblastoma ( pR b) tumor suppressors, as induced by the viral oncogenes large and small T of SV 40, triggers anchorage‐independent growth in RAS , HDAC 4‐ TM and, to a lesser extent, in HDAC 4‐ wild type (WT)‐ expressing cells. Our results suggest an oncogenic function of class II a HDAC s in human cells, and justify further efforts to discover and evaluate isoform‐specific inhibitors of these epigenetic regulators from a therapeutic perspective." @default.
• W2897735072 created "2018-10-26" @default.
• W2897735072 creator A5028266976 @default.
• W2897735072 creator A5066885893 @default.
• W2897735072 creator A5080222062 @default.
• W2897735072 date "2018-11-14" @default.
• W2897735072 modified "2023-09-25" @default.
• W2897735072 title "Unscheduled <scp>HDAC</scp> 4 repressive activity in human fibroblasts triggers <scp>TP</scp> 53‐dependent senescence and favors cell transformation" @default.
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• W2897735072 doi "https://doi.org/10.1002/1878-0261.12392" @default.
• W2897735072 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6275271" @default.
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