Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 113, Issue 7, Pages 2375-2382Publisher
WILEY-BLACKWELL
DOI: 10.1002/jcb.24109
Keywords
TSA; JMJD2B; APOPTOSIS; SURVIVIN; CYCLIN B1; PROSTATE CANCER CELL
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Funding
- National Natural Science Foundation of China [31170719, 30971613, 91019011]
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Histone deacetylase (HDAC) inhibitors are emerging as a novel class of anti-tumor agents and have manifested the ability to induce apoptosis of cancer cells, and a significant number of genes have been identified as potential effectors responsible for HDAC inhibitor-induced apoptosis. However, the mechanistic actions of these HDAC inhibitors in this process remain largely undefined. We here report that the treatment of LNCap prostate cancer cells with HDAC inhibitor trichostatin A (TSA) resulted in downregulation of the Jumonji domain-containing protein 2B (JMJD2B). We also found that the TSA-mediated decrease in survivin expression in LNCap cells was partly attributable to downregulation of JMJD2B expression. This effect was attributable to the promoted degradation of survivin protein through inhibition of Cyclin B1/Cdc2 complex-mediated survivin Thr34 phosphorylation. Consequently, knockdown of JMJD2B enhanced TSA-induced apoptosis by regulating the Cyclin B1-dependent survivin degradation to potentiate the apoptosis pathways. J. Cell. Biochem. 113: 2375-2382, 2012. (C) 2012 Wiley Periodicals, Inc.
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