miR-let-7a suppress cell invasion and migration via the depressing PKM2 in prostatic cancer

Objective: Some cancer reports found that miR-let-7a overexpression could suppress cancer cell biological activities M2 splice isoform of pyruvate kinase (PKM2) down-regulation, however, the correlation between miR-let-7a and PKM2 was unclear in prostatic cancer. The aim of this study was to study the effect and mechanism of miR-let-7a in prostatic cancer. Methods: To evaluate the PKM2 protein expression in adjacent and cancer tissues from 30 prostatic cancer patients by IHC assay and RT-PCR, the and analyzed the correlation between PKM2 and miR-let-7a. In the cell culture experiments, the DU-145 and PC-3 cells which were two representativeness kinds of prostatic cancer cell lines were divided into 3 groups: NC (un-treated) group; BL (the cell were transfected with blank vector) group and miR-let-7a (the cell were transfected with miR-let-7a mimics). The invasion and migration abilities of difference groups were evaluated by transwell and wound healing assay, and measured the relative protein expression (PKM2 and heterogeneous-nuclear ribonucleoprotein A (hnRNPA1) by WB assay. Results: The PKM2 protein expression of cancer tissues were stronger than that of adjacent normal tissues; meanwhile, The miR-let-7a and PKM2 gene expressions were significantly differences between two tissues (P<0.05, respectively), and the miR-let-7a was negatively correlation with PKM2 mRNA expression in cancer tissues (r=-5.3105). In the cell experiments, the invasion cell number of miR-let-7a group was significantly decreased compared with BL group (P<0.05, respectively) and the wound healing rate of miR-let-7a group was significantly down-regulation compared with BL group (P<0.05, respectively). By the WB assay, the PKM2 and hnRNPA1 which were closely correlated with miR-let-7a proteins expression were significantly differences among three groups (P<0.05, respectively). Conclusion: miR-let-7a was known as a supper factor in prostate cancer, miR-let-7a overexpression inhibited the cell invasion and migration abilities via regulation PKM2 and hnRNPA1.