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Cordycepin causes p21WAF1-mediated G2/M cell-cycle arrest by regulating c-Jun N-terminal kinase activation in human bladder cancer cells |
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| Authors: | Se-Jung Lee Si-Kwan Kim Wun-Jae Kim Sung-Kwon Moon |
| Institution: | a Department of Food and Biotechnology, Chungju National University, Chungju, Chungbuk 380-702, South Korea b Personalized Tumor Engineering Research Center, Chungbuk National University, Cheongju, Chungbuk 361-763, South Korea c Department of Life Science, College of Biomedical and Health Science, Konkuk University, Chungju, Chungbuk 380-701, South Korea d Department of Urology, Chungbuk National University College of Medicine, Cheongju, Chungbuk 361-763, South Korea |
| Abstract: | Cordycepin (3′-deoxyadenosine), a bioactive compound of Cordycepsmilitaris, has many pharmacological activities. The present study reveals novel molecular mechanisms for the anti-tumor effects of cordycepin in two different bladder cancer cell lines, 5637 and T-24 cells. Cordycepin treatment, at a dose of 200 μM (IC50) during cell-cycle progression resulted in significant and dose-dependent growth inhibition, which was largely due to G2/M-phase arrest, and resulted in an up-regulation of p21WAF1 expression, independent of the p53 pathway. Moreover, treatment with cordycepin-induced phosphorylation of JNK (c-Jun N-terminal kinases). Blockade of JNK function using SP6001259 (JNK-specific inhibitor) and small interfering RNA (si-JNK1) rescued cordycepin-dependent p21WAF1 expression, inhibited cell growth, and decreased cell cycle proteins. These results suggest that cordycepin could be an effective treatment for bladder cancer. |
| Keywords: | Cordycepin Bladder cancer cells JNK G2/M-phase cell-cycle arrest p21WAF1 |
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