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Repression of NR4A1 by a chromatin modifier promotes docetaxel resistance in PC‐3 human prostate cancer cells
Author(s) -
Yu Liang,
Su Yan-sheng,
Zhao Jie,
Wang He,
Li Wei
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.06.029
Subject(s) - corepressor , cancer research , prostate cancer , histone deacetylase , cancer cell , gene silencing , chromatin remodeling , chemistry , histone , chromatin , gene knockdown , histone deacetylase 2 , docetaxel , microbiology and biotechnology , biology , cancer , transcription factor , nuclear receptor , apoptosis , biochemistry , genetics , dna , gene
Epigenetic silencing mechanisms play an important role in chemoresistance of human cancer. Here we report the upregulated expression of metastasis‐associated protein 1 (MTA1), a component of the nucleosome remodeling deacetylation (NuRD) complex, in chemoresistant prostate cancer (PCa). MTA1 knockdown in PC‐3 cells inhibited cell proliferation and enhanced docetaxel (DTX)‐induced cell death. Conversely, overexpression of MTA1 promotes DTX chemoresistance in PC‐3 cells. MTA1 acted as a potent corepressor of the nuclear receptor NR4A1 transcription by interacting with histone deacetylase 2 (HDAC2). These findings suggest that MTA1 may serve as a novel DTX‐resistance promoter in PC‐3 cells.