MicroRNA-373-3p inhibits prostate cancer progression by targeting AKT1.

Objective: This study aims to investigate whether microRNA-373-3p could inhibit the progression of prostate cancer (PCa) by targeting and degrading AKT1.
Patients and Methods: Expression levels of microRNA-373-3p and AKT1 in PCa tissues and benign prostate hyperplasia (BPN) tissues were detected by quantitative Real-Time-Polymerase Chain Reaction (qRT-PCR). According to the follow-up data, survival curves and receiver operating characteristic (ROC) curves were drawn to investigate whether microRNA-373-3p could be served as a biomarker for early diagnosis and prognosis of PCa. The effect of microRNA-373-3p on cell proliferation was examined by cell counting kit-8 (CCK-8) assay. Subsequently, we explored the direct binding condition of AKT1 and microRNA-373-3p by dual-luciferase reporter gene assay and Western blot.
Results: QRT-PCR results showed that microRNA-373-3p level was significantly lower in PCa tissues compared with that of BPN tissues, whereas AKT1 expression was significantly increased. By analyzing the survival curve and ROC curve, we found that the overall survival (OS) of PCa patients with higher microRNA-373-3p expression was markedly longer than those with lower expression. Besides, microRNA-373-3p could be used as an early diagnostic marker to distinguish PCa from BPH. Overexpression of microRNA-373-3p in PCa cells (LNCaP and PC3 cells) remarkably inhibited cell proliferation. Dual-luciferase reporter gene assay and Western blot showed that microRNA-373-3p targeted the 3'UTR of AKT1 and inhibited its expression.
Conclusions: Downregulated microRNA-373-3p promoted the proliferation of prostate cancer cells via targeting AKT1.