Prostate cancer is the leading cause of cancer deaths among men in the worldwide, it's important to find new prognostic factors and therapeutic targets. microRNAs play critical roles in the development and progression of prostate cancer. Here we revealed miR-1301 promoted prostate cancer progression. miR-1301 was upregulated in prostate cancer tissues and cells, overexpression of miR-1301 promoted anchorage-dependent and -independent growth using MTT analysis, colony formation analysis and soft agar growth analysis, whereas knockdown of miR-1301 suppressed anchorage-dependent and -independent growth. We also found overexpression of miR-1301 inhibited p27 expression and promoted Cyclin D1 expression, whereas knockdown of miR-1301 reduced this effect, suggesting miR-1301 promoted the G1/S transition. These results suggested miR-1301 promoted cell proliferation of prostate cancer. microRNAs can inhibit target mRNA translation or/and induce mRNA degradation, we found tumor suppresser PPP2R2C was the target of miR-1301, simultaneous downregualtion of PPP2R2C and miR-1301 promoted anchorage-dependent and -independent growth. These findings suggested miR-1301 promoted prostate cancer proliferation by inhibiting PPP2R2C, and might a therapeutic target for prostate cancer.
Biomedicine & pharmacotherapy = BiomeĢdecine & pharmacotheĢrapie. 2016 Apr 08 [Epub]
Dongbin Bi, Hao Ning, Shuai Liu, Xinxiang Que, Kejia Ding
Department of Urology, Provincial Hospital affiliated to Shandong University, 324 Jingwu Street, Jinan 250021, PR China., Department of Urology, Provincial Hospital affiliated to Shandong University, 324 Jingwu Street, Jinan 250021, PR China., Department of Urology, Provincial Hospital affiliated to Shandong University, 324 Jingwu Street, Jinan 250021, PR China., Department of Urology, Provincial Hospital affiliated to Shandong University, 324 Jingwu Street, Jinan 250021, PR China., Department of Urology, Provincial Hospital affiliated to Shandong University, 324 Jingwu Street, Jinan 250021, PR China. Electronic address: .