Upregulated wnt-11 and mir-21 expression trigger epithelial mesenchymal transition in aggressive prostate cancer cells

Arisan, E.D., Rencuzogullari, O., Freitas, I.L., Radzali, S., Keskin, B., Kothari, A., Warford, A. and Uysal-Onganer, P. 2020. Upregulated wnt-11 and mir-21 expression trigger epithelial mesenchymal transition in aggressive prostate cancer cells. Biology. 9 (3) 52. https://doi.org/10.3390/biology9030052

TitleUpregulated wnt-11 and mir-21 expression trigger epithelial mesenchymal transition in aggressive prostate cancer cells
TypeJournal article
AuthorsArisan, E.D., Rencuzogullari, O., Freitas, I.L., Radzali, S., Keskin, B., Kothari, A., Warford, A. and Uysal-Onganer, P.
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.

KeywordsmicroRNA; in situ hybridization; prostate cancer; Wnt-11; miR-21
Article number52
JournalBiology
Journal citation9 (3)
ISSN2079-7737
Year2020
PublisherMDPI
Publisher's version
License
CC BY 4.0
File Access Level
Open (open metadata and files)
Digital Object Identifier (DOI)https://doi.org/10.3390/biology9030052
Publication dates
Published09 Mar 2020

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