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

BMC Complementary and Alternative Medicine

Research Article

Yong-bin Meng¹  Xiao-feng Zhai¹  Yu-yu Guo¹  Zhe Chen¹  Qun Liu¹  Fan-fu Fang² 

[1] Department of Integrative Oncology, Changhai Hospital of Traditional Chinese Medicine, Second Military Medical University, 200433, Shanghai, China;Department of Rehabilitation Medicine, Changhai Hospital of Traditional Chinese Medicine, Second Military Medical University, 200433, Shanghai, China;

关键词: miR-181a;    Bufalin;    Apoptosis;    Prostate cancer;    Traditional Chinese medicine;   

DOI  :  10.1186/1472-6882-13-325

 received in 2013-07-21, accepted in 2013-11-18,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundBufalin 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.MethodsApoptosis 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.ResultsBufalin 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.ConclusionsOur 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.

【 授权许可】

Unknown   
© Zhai et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.