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Repression of NR4A1 by a chromatin modifier promotes docetaxel resistance in PC-3 human prostate cancer cells.

Abstract
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.
AuthorsLiang Yu, Yan-sheng Su, Jie Zhao, He Wang, Wei Li
JournalFEBS letters (FEBS Lett) Vol. 587 Issue 16 Pg. 2542-51 (Aug 19 2013) ISSN: 1873-3468 [Electronic] England
PMID23831020 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Chemical References
  • Chromatin
  • Mta1 protein, human
  • NR4A1 protein, human
  • Nuclear Receptor Subfamily 4, Group A, Member 1
  • Repressor Proteins
  • Taxoids
  • Trans-Activators
  • Docetaxel
  • Histone Deacetylase 2
  • Histone Deacetylases
  • Mi-2 Nucleosome Remodeling and Deacetylase Complex
Topics
  • Animals
  • Apoptosis
  • Cell Death
  • Cell Line, Tumor
  • Cell Survival
  • Chromatin (chemistry)
  • Docetaxel
  • Drug Resistance, Neoplasm
  • Epigenesis, Genetic
  • Gene Expression Regulation, Neoplastic
  • Histone Deacetylase 2 (metabolism)
  • Histone Deacetylases (metabolism)
  • Humans
  • Male
  • Mi-2 Nucleosome Remodeling and Deacetylase Complex (metabolism)
  • Mice
  • Mice, Nude
  • Neoplasm Transplantation
  • Nuclear Receptor Subfamily 4, Group A, Member 1 (metabolism)
  • Prostatic Neoplasms (metabolism)
  • Protein Binding
  • Repressor Proteins (metabolism)
  • Taxoids (pharmacology)
  • Trans-Activators
  • Transcription, Genetic

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