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Experimental and Molecular Therapeutics 7: Identification of Drug Resistance Mechanisms

Inactivation of Id1 increases taxol-induced apoptosis in androgen independent prostate cancer cells through activation of JNK signaling pathway

Y. C. Wong, Xiao Meng Zhang, M. T. Ling and X. H. Wang
Y. C. Wong
University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region of China
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Xiao Meng Zhang
University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region of China
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M. T. Ling
University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region of China
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X. H. Wang
University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region of China
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DOI:  Published April 2006
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Proc Amer Assoc Cancer Res, Volume 47, 2006

Abstract

1265

Resistance to anticancer drugs is the major problem in the treatment of many advanced cancers including androgen-independent prostate cancer. Recently, increased expression of Id-1, a basic helix-loop-helix protein, is reported in several types of advanced cancer. It is suggested that high expression of Id-1 may provide an advantage for cancer cell survival and inactivation of Id-1 may be able to increase cancer cells’ susceptibility to apoptosis. To test this hypothesis, in this study, using RNA interfering technology, we inactivated the Id-1 gene in two androgen-independent prostate cancer cell lines, DU145 and PC3, and investigated if downregulation of Id-1 could lead to increased sensitivity to a commonly used anticancer drug, taxol. Using colony forming and MTT assays, we found that inactivation of Id-1 resulted in both decreased colony forming ability and cell viability in prostate cancer cells after taxol treatment. In addition, the si-Id-1 induced sensitization to taxol was associated with activation of apoptosis pathway demonstrated by increased apoptotic index, DNA laddering, sub-G1 phase of the cell cycle, as well as cleaved-PARP and Caspase 3. Furthermore, c-Jun N-terminal kinase (JNK), one of the common pathways responsible for taxol-induced apoptosis, was also activated in the si-Id-1 transfected cells. Inhibition of JNK activity by a specific inhibitor, SP600125, blocked the si-Id-1-induced sensitivity to taxol. These results indicate that increased Id-1 expression in prostate cancer cells may play a protective role against apoptosis, and downregulation of Id-1 may be a potential target to increase sensitivity of taxol-induced apoptosis in prostate cancer cells.(Supported by RGC grants:HKU7314/01M, hku7490/03M, HKU7470/04M, HKU7478/03M)

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Cancer Research: 66 (8 Supplement)
April 2006
Volume 66, Issue 8 Supplement
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Inactivation of Id1 increases taxol-induced apoptosis in androgen independent prostate cancer cells through activation of JNK signaling pathway
Y. C. Wong, Xiao Meng Zhang, M. T. Ling and X. H. Wang
Cancer Res April 15 2006 (66) (8 Supplement) 299;

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Inactivation of Id1 increases taxol-induced apoptosis in androgen independent prostate cancer cells through activation of JNK signaling pathway
Y. C. Wong, Xiao Meng Zhang, M. T. Ling and X. H. Wang
Cancer Res April 15 2006 (66) (8 Supplement) 299;
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Cancer Research Online ISSN: 1538-7445
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