MicroRNA MiR-490-5p suppresses pancreatic cancer through regulating epithelial-mesenchymal transition via targeting MAGI2 antisense RNA 3

13Citations
Citations of this article
6Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Pancreatic cancer with about 5% five-year overall survival rate remains a challenge. Invasion and migration of pancreatic cancer cells are the main factors leading to poor prognosis. MicroRNA-490-5p (miR-490-5p) has anti-cancer effects in a variety of tumors, but its role in pancreatic cancer has not been reported. The mRNA expressions of miR-490-5p, MAGI2 antisense RNA 3 (MAGI2-AS3), Matrix metalloproteinase (MMP)2, MMP9, N-cadherin, and E-cadherin were detected by quantitative real-time PCR, while the protein expressions of these genes except miR-490-5p were measured by Western blot analysis. The cell viability, apoptosis, migration and invasion were detected by cell counting kit-8 (CCK-8), apoptosis and transwell assays. MiR-490-5p was abnormally low-expressed in pancreatic cancer, whose down-regulation generated enhanced effects on viability, migration and invasion in pancreatic cancer cells, as well as MAGI2-AS3 expression. MiR-490-5p mimic exerted the opposite effect on cells, which also down-regulated MMP2, MMP9, and N-cadherin protein expressions, while up-regulating E-cadherin protein expression. MAGI2-AS3, which was the targeted binding site of miR-490-5p, promoted viability, migration and invasion, and inhibited apoptosis of cancer cells. More importantly, miR-490-5p played an anti-cancer role in pancreatic cancer by targeting MAGI2-AS3 and regulating epithelial–mesenchymal transition (EMT), which was partially offset by MAGI2-AS3.

Cite

CITATION STYLE

APA

Xu, Z., Chen, Z., Peng, M., Zhang, Z., Luo, W., Shi, R., … Hong, Y. (2022). MicroRNA MiR-490-5p suppresses pancreatic cancer through regulating epithelial-mesenchymal transition via targeting MAGI2 antisense RNA 3. Bioengineered, 13(2), 2673–2685. https://doi.org/10.1080/21655979.2021.2024653

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free