Abstract

Prostate cancer (PCa) is the second-leading cause of cancer-related death among men. microRNAs have been identified as having potential roles in tumorigenesis. An oncomir, miR-21, is commonly highly upregulated in many cancers, including PCa, and showed correlation with the Wnt-signaling axis to increase invasion. Wnt-11 is a developmentally regulated gene and has been found to be upregulated in PCa, but its mechanism is unknown. The present study aimed to investigate the roles of miR-21 and Wnt-11 in PCa in vivo and in vitro. First, different Gleason score PCa tissue samples were used; both miR-21 and Wnt-11 expressions correlate with high Gleason scores in PCa patient tissues. This data then was confirmed with formalin-fixed paraffin cell blocks using PCa cell lines LNCaP and PC3. Cell survival and colony formation studies proved that miR-21 involves in cells’ behaviors, as well as the epithelial-mesenchymal transition. Consistent with the previous data, silencing miR-21 led to significant inhibition of cellular invasiveness. Overall, these results suggest that miR-21 plays a significant role related to Wnt-11 in the pathophysiology of PCa.

Highlights

  • Prostate cancer (PCa) is the development of carcinoma within the prostate gland of the male reproductive system

  • We reveal that silencing miR-21 expression results in significant inhibition of cellular invasiveness

  • In this study, we showed that miR-21 plays an important role during cell migration and invasion

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Summary

Introduction

Prostate cancer (PCa) is the development of carcinoma within the prostate gland of the male reproductive system. It is a heterogeneous disease and may present itself as an indolent or aggressive form [1]. There is no specific form of screening for PCa, and health practitioners may use a combination of several tests in order to diagnose a patient. Tumors with lower GS indicate cells that are similar to normal cells and are likely to be less aggressive. Those assigned with higher scores are indicative of tumors with poorly

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