Research Article

MicroRNA-16 Represses TGF-β1-induced Epithelial-to-Mesenchymal Transition in Human Lung Adenocarcinoma Cell Line

Author(s): Subbiah Rajasekaran*, Sehal Mishra and Deepa Gandhi

Volume 11, Issue 3, 2022

Published on: 06 October, 2022

Page: [206 - 215] Pages: 10

DOI: 10.2174/2211536611666220826124058

Price: $65

Abstract

Background: The transforming growth factor-beta1 (TGF-β1)-induced epithelial-tomesenchymal transition (EMT) has a crucial effect on the progression and metastasis of lung cancer cells.

Objective: The purpose of this study was to investigate whether microRNA (miR)-16 can suppress TGF-β1-induced EMT and proliferation in human lung adenocarcinoma cell line (A549).

Methods: Quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-16. The hallmarks of EMT were assessed by RT-qPCR, Western blotting, and cell proliferation assay. A bioinformatics tool was used to identify the putative target of miR-16. The activation of TGF-β1/Smad3 signaling was analysed using Western blotting.

Results: Our results showed that miR-16 expression was significantly down-regulated by TGF-β1 in A549 cells. Moreover, agomir of miR-16 suppressed TGF-β1-induced EMT and cell proliferation. Computational algorithms predicted that the 3’-untranslated regions (3’-UTRs) of Smad3 are direct targets of miR-16. In addition, miR-16 mimic was found to inhibit the TGF-β1-induced activation of the TGF-β1/Smad3 pathway, suggesting that miR-16 may function partly through regulating Smad3.

Conclusion: Our results demonstrated that overexpression of miR-16 suppressed the expression and activation of Smad3, and ultimately inhibited TGF-β1-induced EMT and proliferation in A549 cells. The present findings support further investigation of the anti-cancer effect of miR-16 in animal models of lung cancer to validate the therapeutic potential.

Keywords: Adenocarcinoma, A549 cell line, cell proliferation, EMT, miR-16, TGF-β1.

Graphical Abstract
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