Open Access

ARTICLE

Circular RNA circFOXM1 triggers the tumorigenesis of non-small cell lung cancer through miR-132-3p/TMEM14A axis

WEIGAO ZHONG^1,*, AIQIN CHEN², XIAOHONG TANG¹, YI LIU¹

1 Department of Respiratory, Sichuan Mianyang 404 Hospital, Mianyang, 621000, China
2 Department of Electrocardiogram Room, Wuxi Puren Medical Group, Wuxi, 214000, China

* Corresponding Author: Weigao Zhong. Email:

BIOCELL 2021, 45(4), 901-910. https://doi.org/10.32604/biocell.2021.08672

Received 23 September 2019; Accepted 13 May 2020; Issue published 22 April 2021

Abstract

Earlier studies indicated that circular RNAs (circRNAs) were found in various cancer cells, and circFOXM1 was reported to act as an oncogene in non-small cell lung cancer (NSCLC). However, the function of circFOXM1 in NSCLC remains unclear. The expression levels of genes were measured using quantitative real-time polymerase chain reactions (qRT-PCR). Cell proliferation and apoptosis were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide solution (MTT) and flow cytometry assay. The relative protein expression was assessed by western blot. Moreover, transwell assays were employed to examine cell migration and invasion. The targeted relationship was confirmed by dual-luciferase reporter assay. The expression of circFOXM1 was up-regulated in NSCLC tissues and cell lines. The depletion of circFOXM1 decreased the proliferation, migration, invasion, and induced cell apoptosis of NSCLC cells. MicroRNA-132-3p (MiR-132-3p) was identified as a target of circFOXM1. The expression level of miR-132-3p was decreased in NSCLC tissues and cell lines and inversely correlated with circFOXM1 expression. Furthermore, the effects of circFOXM1 down-regulation on NSCLC cell progression were abolished by miR-132-3p inhibitor. Transmembrane protein 14A (TMEM14A) was verified as a target gene of miR-132-3p. The effects of circFOXM1 depletion on NSCLC cell proliferation, apoptosis, migration, and invasion were reversed by TMEM14A overexpression. Our study demonstrated that knockdown of circFOXM1 suppressed NSCLC progression through regulating miR-132-3p/TMEM14A axis, suggesting the circFOXM1/miR-132-3p/TMEM14A axis may serve as the novel target for NSCLC diagnosis and therapy.

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