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Liu Leiyu, Zao Binjiahui, Qin Wei, Chen Yuanyuan, Lin Feng, Zou Haifeng, Yu Xiaoguang. Transfection of PDCD5 Promotes Effects of Cisplatin on Apoptosis-inducing of Prostate Cancer Cells[J]. Cancer Research on Prevention and Treatment, 2012, 39(01): 32-35. DOI: 10.3971/j.issn.1000-8578.2012.01.008
Citation: Liu Leiyu, Zao Binjiahui, Qin Wei, Chen Yuanyuan, Lin Feng, Zou Haifeng, Yu Xiaoguang. Transfection of PDCD5 Promotes Effects of Cisplatin on Apoptosis-inducing of Prostate Cancer Cells[J]. Cancer Research on Prevention and Treatment, 2012, 39(01): 32-35. DOI: 10.3971/j.issn.1000-8578.2012.01.008

Transfection of PDCD5 Promotes Effects of Cisplatin on Apoptosis-inducing of Prostate Cancer Cells

  • Objective To investigate the effects of PDCD5 overexpression on apoptosis of human prostate cancer DU145 cells induced by cisplatin. Methods First,the proliferation of the DU145 cells treated with cisplatin was assayed by CCK-8.Secondly,we established stably transfected DU145 cells overexpressing PDCD5.Then,apoptosis was determined by Annexin V-FITC & PI double staining and electron microscopy,and the expression of apoptosis-related proteins was detected by western blot. Results Cisplatin inhibited cell proliferation of prostate cancer DU145 cells on a dose- and time-dependent manner.Stably transfected DU145 cells with PDCD5 overexpression were successfully established.As shown in flow cytometric analysis and electron microscopy images the apoptosis of DU145 cells treated with PDCD5 and cisplatin (25 μmol/L) was increased markedly compared with the cells treated with PDCD5 and cisplatin(10 μmol/L) or the cells treated with cisplatin alone.Western blot analysis suggested that the level of Bcl-2 expressed in the DU145 cells treated with PDCD5 and cisplatin was decreased obviously,while Bax protein level showed no significant difference. Conclusion Although PDCD5 overexpression alone does not cause apoptosis in DU145 cells,it can largely enhance the apoptosis-promoting effect of cisplatin on DU145 cells.The mechanism is involved in reducing the expression ratio of Bcl-2/Bax.
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