The putative tumour suppressor miR-1-3p modulates prostate cancer cell aggressiveness by repressing E2F5 and PFTK1.

摘要: Previous studies report that miR-1-3p, a member of the microRNA-1 family (miR-1), and functions as tumor suppressor in several different cancers. However, little is known regarding biological role intrinsic regulatory mechanisms miR-1-3p prostate cancer (PCa). In this study, expression levels were first examined PCa cell lines tissues by RT-qPCR bioinformatics. The vitro vivo functional effect was further. A luciferase reporter assay conducted to confirm target associations. We found significantly downregulated advanced lines. Low strongly associated with aggressive clinicopathological features poor prognosis patients. Ectopic 22RV1 LncaP cells sufficient prevent growth cycle progression vivo. Further mechanistic revealed could directly mRNA 3′- untranslated region (3′- UTR) two central genes, E2F5 PFTK1, suppress their protein expression. addition, knockdown PFTK1 mimicked tumor-suppressive effects overexpression on progression. Conversely, concomitant substantially reversed inhibitory either or silencing alone. These data highlight an important for regulation proliferation molecular etiology indicate potential applications furthering prognostics therapeutics.