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TSA‐induced JMJD2B downregulation is associated with cyclin B1‐dependent survivin degradation and apoptosis in LNCap cells
Author(s) -
Zhu Shan,
Li Yueyang,
Zhao Li,
Hou Pingfu,
Shangguan Chenyan,
Yao Ruosi,
Zhang Weina,
Zhang Yu,
Tan Jiang,
Huang Baiqu,
Lu Jun
Publication year - 2012
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24109
Subject(s) - survivin , downregulation and upregulation , lncap , apoptosis , microbiology and biotechnology , degradation (telecommunications) , cancer research , chemistry , biology , medicine , computer science , biochemistry , prostate cancer , cancer , gene , telecommunications
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. © 2012 Wiley Periodicals, Inc.