Effects of miR-132-3p on progress and epithelial mesenchymal transition of non-small cell lung cancer via regulating KLF7.

Abstract

BACKGROUND:

MicroRNAs (miRNAs) often appear as oncogenes or tumor suppressor genes. The aim of this research was to examine miR-132-3p and Kruppel-like factor 7 (KLF7) effects in the development of non-small cell lung cancer (NSCLC).

METHODS:

We used quantitative reverse transcription polymerase chain reaction (qRT-PCR) to determine miR-132-3p expression in tissue specimens and 6 cells (A549, H1650, H292, H1299, H1944, BEAS-2b). Luciferase report forecasted the targeting relationship between miR-132-3p and KLF7. The expression of KLF7 and interstitial protein was determined by western blot. Proliferation test and Transwell assay were adopted for examining cell development. The Cell Counting Kit-8 (CCK-8) colorimetric method was used to observe the effects of miR-132-3p and KLF7 on the proliferation, metastasis, and invasion of NSCLC tumor cells. In order to determine whether the metastasis of NSCLC tumor cells was epithelial-mesenchymal transition (EMT)-mediated, supplementary experiments with E-cadherin and vimentin were performed.

RESULTS:

An increased expression of miR-132-3p was detected in NSCLC. Its mimic promoted the proliferation of tumor cells. As an immediate site of miR-132-3p, KLF7 was reversely adjusted via miR-132-3p and restrained the development of tumor cells in NSCLC, the effects of which were attenuated via KLF7 over-expression. Besides, the presence of EMT-related diversions was confirmed in NSCLC.

CONCLUSIONS:

By targeting KLF7, miR-132-3p was capable of promoting the proceeding of NSCLC tumor cells. We discovered miR-132-3p/KLF7 route may exhibit curative target for NSCLC.

• Authors: Ning Wang, Ye Xu, Qingkui Guo, Chen Zhu, Wen Zhao, Wenliang Qian, Min Zheng
• Journal: Journal of thoracic disease (J Thorac Dis) Vol. 13 Issue 4 Pg. 2426-2436 (Apr 2021) ISSN: 2072-1439 [Print] China
• PMID: 34012590 (Publication Type: Journal Article)
• Copyright: 2021 Journal of Thoracic Disease. All rights reserved.