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標題: Retinoic Acid Induces Apoptosis of Prostate Cancer DU145 Cells through Cdk5 Overactivation
作者: Chen, Mei-Chih
Huang, Chih-Yang
Hsu, Shih-Lan
Lin, Eugene
Ku, Chien-Te
Lin, Ho
Chen, Chuan-Mu
Project: Evidence-Based Complementary and Alternative Medicine, Volume 2012
Retinoic 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.
DOI: 10.1155/2012/580736
Appears in Collections:生命科學系所

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