Open Access

ARTICLE

LINC00609 inhibits A549 cells progression through the regulation of miR-128-3p/RND3 axis

XIANGCHAO DING^1,#, YANG ZHAO^2,#, XINGHUA ZHANG¹, HUIQING LIN^1,*

1 Department of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan, 430060, China
2 Department of Respiratory and Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, 430060, China

* Corresponding Author: HUIQING LIN. Email:
# Co-first authors: Xiangchao Ding, Yang Zhao

BIOCELL 2023, 47(5), 1117-1126. https://doi.org/10.32604/biocell.2023.026715

Received 21 September 2022; Accepted 26 December 2022; Issue published 10 April 2023

Abstract

Background: Long-chain non-coding RNA (lncRNA) LINC00609 is a potential tumor suppressor, but the mechanism of action in non-small cell lung cancer (NSCLC) is yet to be understood.Objectives: The effects of LINC00609 on A549 cell proliferation, apoptosis, and cell cycle arrest were investigated. Methods: The LINC00609 levels in NSCLC and normal tissues were analyzed by bioinformatics. Expressions of LINC00609, miR-128-3p, and Rho family GTPase 3 (RND3) in NSCLC cells (A549) were determined by qRT-PCR. Bioinformatics analysis predicted target genes and dual-luciferase reporter assays to ensure that LINC00609 targeted miR-128-3p and miR-128-3p targeted RND3. The proliferation of cells was determined using EDU and CCK-8. Flow cytometry was used to evaluate cell apoptosis rate and cell cycle. The western blotting assay identified proteins related to proliferation and apoptosis. Results: In NSCLC tissues, LINC00609 was expressed in low levels, while its high expression was associated with a higher survival rate. LINC00609 affected cell proliferation, apoptosis, cell cycle arrest, and expression of related proteins. Dual-luciferase reporter assay showed that LINC00609 binds specifically to miR-128-3p, and miR-128-3p binds to RND3. MiR-128-3p overexpression could neutralize the effects of LINC00609. A siRNA targeting RND3 could reverse the effect of the miR-128-3p inhibitor. Silencing RND3 resulted in a decrease in apoptosis rate and the number of cells in the S-phase and an increase in the number of cells in the G1-phase. Furthermore, phosphorylation levels of the AKT protein and mTOR protein, and Bcl2 expression, increased; however, the expression of RND3, Bax, and caspase3 decreased. Conclusions: LINC00609 regulated miR-128-3p/RND3 axis to modulate A549 cell proliferation, apoptosis, and cell cycle arrest. In the case of NSCLC, LINC00609 could be a potential target for therapy.

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