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MiR-181a contributes to bufalin-induced apoptosis in PC-3 prostate cancer cells

Xiaofeng ZhaiDepartment of Integrative Oncology, Changhai Hospital of Traditional Chinese Medicine, Second Military Medical University, Shanghai 200433, China. [email protected]Fanfu FangDepartment of Rehabilitation Medicine, Changhai Hospital of Traditional Chinese Medicine, Second Military Medical University, Shanghai, 200433, ChinaQun LiuDepartment of Integrative Oncology, Changhai Hospital of Traditional Chinese Medicine, Second Military Medical University, Shanghai, 200433, ChinaYongbin MengDepartment of Integrative Oncology, Changhai Hospital of Traditional Chinese Medicine, Second Military Medical University, Shanghai, 200433, ChinaYuyu GuoDepartment of Integrative Oncology, Changhai Hospital of Traditional Chinese Medicine, Second Military Medical University, Shanghai, 200433, ChinaZhe ChenDepartment of Integrative Oncology, Changhai Hospital of Traditional Chinese Medicine, Second Military Medical University, Shanghai, 200433, China
2013en
ABI

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BACKGROUND: Bufalin is a major active compound of cinobufacini, which comes from dried toad venom and has been used for treatments of various cancers in China for many years. A number of studies have demonstrated that bufalin can induce apoptosis in some cancers. However, effects and mechanism of bufalin on prostate cancer cells remain unknown. METHODS: Apoptosis assay was measured by the annexin-V/PI flow cytometric assay. Western blot was used to measure Caspase-3 and Bcl-2. qRT-PCR was used to measure the relative expression of miR-181a. RESULTS: Bufalin was found to induce the expression of miR-181a, a small non-coding RNA believed to induce apoptosis by repressing its target gene, BCL-2. In prostate cancer PC-3cell line, bufalin-induced apoptosis can be largely attenuated by a miR-181a inhibitor, which blocked bufalin-induced Bcl-2 reduction and caspase-3 activation. CONCLUSIONS: Our dataindicatedthat miR-181a mediates bufalin-induced apoptosis in PC-3 cells. Thus, we presented here a new pharmacological mechanism for bufalin in anti-tumor therapy.

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