The Suppression of the Epithelial to Mesenchymal Transition in Prostate Cancer - through the Targeting of MYO6 Using MiR-145-5p

Sep 21, 2026

Aberrant expression of miR-145-5p has been linked to prostate cancer, where it is suggested to act as a tumor suppressor. In other cancers, miR-145-5p inhibits epithelial-to-mesenchymal transition (EMT), a key driver of progression. This study used in silico and in vitro analyses to define the miR-145-5p–EMT axis in prostate cancer, identifying MYO6 as a validated target. miR-145-5p inhibition or overexpression affected proliferation, clonogenicity, migration, EMT marker expression, and suggested recurrence prediction.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages20

Reading Time50 min

AccessFree to download

Introduction

Prostate cancer and EMT as a driver of metastasis

MicroRNAs and post-transcriptional gene regulation

miR-145-5p rationale and prior evidence

Role across multiple cancer types

Objectives and study approach

Article The Suppression of the Epithelial to Mesenchymal Transition in Prostate Cancer through the Targeting of MYO6 Using MiR-145-5p Lee Armstrong, Colin E. Willoughby and Declan J. McKenna * Citation: Armstrong, L.; Willoughby, C.E.; McKenna, D.J. The Suppression of the Epithelial to Mesenchymal Transition in Prostate Cancer through the Targeting of MYO6 Using MiR-145-5p. Int. J. Mol. Sci. 2024, 25, 4301. [https://doi.org/10.3390/](https://doi.org/10.3390/)[ ](https://doi.org/10.3390/)ijms25084301 Academic Editor: Kexin Xu Received: 19 March 2024 Revised: 9 April 2024 Accepted: 11 April 2024 Published: 12 April 2024 Copyright: © 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ([https://](https://)[ ](https://)[creativecommons.org/licenses/by/](creativecommons.org/licenses/by/)[ ](creativecommons.org/licenses/by/)[4.0/](4.0/)) . Genomic Medicine Research Group, Ulster University, Cromore Road, Coleraine BT52 1SA, UK; [armstrong-l16@ulster.ac.uk](armstrong-l16@ulster.ac.uk) (L.A.); [c.willoughby@ulster.ac.uk](c.willoughby@ulster.ac.uk) (C.E.W.) * [Correspondence: dj.mckenna@ulster.ac.uk](Correspondence: dj.mckenna@ulster.ac.uk) Abstract: Aberrant expression of miR-145-5p has been observed in prostate cancer where is has been suggested to play a tumor suppressor role. In other cancers, miR-145-5p acts as an inhibitor of epithelial-to-mesenchymal transition (EMT), a key molecular process for tumor progression. However, the interaction between miR-145-5p and EMT remains to be elucidated in prostate cancer. In this paper the link between miR-145-5p and EMT in prostate cancer was investigated using a combination of in silico and in vitro analyses. miR-145-5p expression was signiﬁcantly lower in prostate cancer cell lines compared to normal prostate cells. Bioinformatic analysis of The Cancer Genome Atlas prostate adenocarcinoma (TCGA PRAD) data showed signiﬁcant downregulation of miR-145-5p in prostate cancer, correlating with disease progression. Functional enrichment analysis signiﬁcantly associated miR-145-5p and its target genes with EMT. MYO6, an EMT-associated gene, was identiﬁed and validated as a novel target of miR-145-5p in prostate cancer cells. In vitro manipulation of miR-145-5p levels signiﬁcantly altered cell proliferation, clonogenicity, migration and expression of EMT-associated markers. Additional TCGA PRAD analysis suggested miR-145-5p tumor expression may be useful predictor of disease recurrence. In summary, this is the ﬁrst study to report that miR-145-5p may inhibit EMT by targeting MYO6 in prostate cancer cells. The ﬁndings suggest miR-145-5p could be a useful diagnostic and prognostic biomarker for prostate cancer. Keywords: prostate cancer; microRNA; miR-145-5p; epithelial-to-mesenchymal transition; MYO6; biomarker 1. Introduction Prostate cancer is a heterogeneous disease affecting millions of men worldwide, predominantly in regions with a high human development index [1] . Epithelial-to-mesenchymal transition (EMT) is a key biological process required for the progression and metastasis of prostate cancer [2] . EMT is a dynamic process in which epithelial cells are reprogrammed to exhibit a mesenchymal phenotype. The loss of cell polarity and cell–cell adhesion leads to enhanced migratory capacity, invasiveness, and resistance to apoptosis [3] . Multiple factors regulate the EMT process, including several miRNAs [4] . MicroRNAs (miRNAs) are short, non-coding RNA molecules that play an important role in regulating gene expression atthe post-transcriptional level. miRNAs bind to speciﬁc sequences in the 30 untranslated region (30 UTR) of their target messenger RNAs (mRNAs), resulting in either mRNA degradation or translational repression [5] . By inhibiting the translation of target mRNAs or causing their degradation, miRNAs can effe

FAQs

What is the main biological process investigated in this article?

The article focuses on epithelial-to-mesenchymal transition (EMT), which supports prostate cancer progression and metastasis.

How does miR-145-5p relate to EMT in prostate cancer?

The study tests whether miR-145-5p can suppress EMT in prostate cancer and explores the underlying molecular interaction.

Which gene is identified as a target of miR-145-5p?

MYO6 is identified and validated as a novel target of miR-145-5p in prostate cancer cells.

Sep 21, 2026

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