MiR-373 Inhibits the Epithelial-Mesenchymal Transition of Prostatic Cancer via Targeting Runt-Related Transcription Factor 2.

Abstract

Prostatic cancer (PCa) is a prevalent form of malignancy based on its high associated levels of mortality and morbidity across the world. MicroRNAs (miRNAs) are significant in the advancement of prostatic cancer. The current study is aimed at exploring the potential roles of miR-373 in PCa. In turn, the study conducted a qRT-PCR test to determine the levels of mRNA. A western blot test was also executed in determining the protein level. The processes of transwell assay and wound healing were integrated in the detection of the potential for PCa cells to invade and migrate. The integration of dual luciferase reporter assay is critical in determining the levels of luciferase activity among prostatic cancer cells. Then, the results showed a net decrease of miR-373 within prostatic cancer cells and tissues. Upregulated miR-373 reduced the invasion and migration potential of PCa cells. Moreover, overexpressed miR-373 increased the levels of E-cadherin and FSP1 as epithelial cell markers. Similarly, the overregulation of miR-373 brought about the upregulation of mesenchymal markers (N-cadherin, Snail, and vimentin). The study predicted runt-related transcription factor 2 (RUNX2) to be a target of miR-373. The luciferase activity of PCa cells was decreased after the cotransfection with miR-373 mimics and RUNX2 3′ untranslated region (3′UTR) wild type (WT). Moreover, RUNX2 became upregulated in PCa cells and tissues. The upregulation of miR-373 decreased the mRNA and protein level of RUNX2. However, overexpressed RUNX2 abated the roles of miR-373 in the intrusion and migration of PCa cells and in regulating the expression of epithelial cell markers and mesenchymal markers. In short, miR-373 may regulate the EMT of PCa cells via targeting RUNX2. The miR-373/RUNX2 axis provides a therapeutic target for PCa.