Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/38567
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dc.contributor.authorChen, Mei-Chihen_US
dc.contributor.authorHuang, Chih-Yangen_US
dc.contributor.authorHsu, Shih-Lanen_US
dc.contributor.authorLin, Eugeneen_US
dc.contributor.authorKu, Chien-Teen_US
dc.contributor.authorLin, Hoen_US
dc.contributor.authorChen, Chuan-Muen_US
dc.date2012-12zh_TW
dc.date.accessioned2014-06-06T08:00:56Z-
dc.date.available2014-06-06T08:00:56Z-
dc.identifier.urihttp://hdl.handle.net/11455/38567-
dc.description.abstractRetinoic acid (RA) has been believed to be an anticancer drug for a long history.However, the molecularmechanisms of RA actions on cancer cells remain diverse. In this study, the dose-dependent inhibition of RA on DU145 cell proliferation was identified. Interestingly, RA treatment triggered p35 cleavage (p25 formation) and Cdk5 overactivation, and all could be blocked by Calpain inhibitor, Calpeptin (CP). Subsequently, RA-triggered DU145 apoptosis detected by sub-G1 phase accumulation and Annexin V staining could also be blocked by CP treatment. Furthermore, RA-triggered caspase 3 activation and following Cdk5 overactivation were destroyed by treatments of both CP and Cdk5 knockdown. In conclusion, we report a new mechanism in which RA could cause apoptosis of androgen-independent prostate cancer cells through p35 cleavage and Cdk5 over-activation. This finding may contribute to constructing a clearer image of RA function and bring RA as a valuable chemoprevention agent for prostate cancer patients.en_US
dc.language.isoen_USzh_TW
dc.relationEvidence-Based Complementary and Alternative Medicine, Volume 2012en_US
dc.relation.urihttp://dx.doi.org/10.1155/2012/580736en_US
dc.titleRetinoic Acid Induces Apoptosis of Prostate Cancer DU145 Cells through Cdk5 Overactivationen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1155/2012/580736zh_TW
dc.contributor.catalogerWei Chun Wangen_US
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