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

• Published in: BMC complementary and alternative medicine Vol. 13; no. 1; p. 325
• Main Authors: Zhai, Xiao-feng, Fang, Fan-fu, Liu, Qun, Meng, Yong-bin, Guo, Yu-yu, Chen, Zhe
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 23.11.2013; BioMed Central
• Subjects: Angiogenesis; Antineoplastic Agents - pharmacology; Apoptosis; Apoptosis - drug effects; Apoptosis - genetics; Bufanolides - pharmacology; Cancer; Cancer cells; Cancer therapies; Care and treatment; Caspase 3 - metabolism; Cell cycle; Cell growth; Cell Line, Tumor; Chinese medicine; Drug resistance; FDA approval; Flow Cytometry; Gene expression; Gene Expression - drug effects; Genes; Hospitals; Humans; Male; MicroRNAs - analysis; MicroRNAs - antagonists & inhibitors; MicroRNAs - genetics; MicroRNAs - metabolism; Oncology, Experimental; Physiological aspects; Prostate cancer; Prostatic Neoplasms - drug therapy; Prostatic Neoplasms - genetics; Prostatic Neoplasms - metabolism; Proteins; Proto-Oncogene Proteins c-bcl-2 - metabolism; Studies; Tumorigenesis; China
• ISSN: 1472-6882; 1472-6882
• DOI: 10.1186/1472-6882-13-325

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. 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. 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. 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.