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Hindi ARHGAP11A Promotes Lung Adenocarcinoma Proliferation and Invasion through ROCK-LIMK-Cofilin Pathway
*Corresponding Author:
Copyright: © 2021 . This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background: We aimed to investigate the clinical significance and biological roles of ARHGAP11A in lung adenocarcinoma (LUAD). Methods: We firstly analyzed the expression level of ARHGAP11A in LUAD based on TCGA. Next, quantitative reverse transcription PCR (qRT-PCR) was performed to examine the expression level of ARHGAP11A in LUAD cell lines (A549, and Calu-3). After ARHGAP11A knockdown in A549 cells, cell counting kit-8 (CCK-8) and trans well assays were used to measure the proliferation and migration ability of A549 cells with or without ARHGAP11A silence. Western blotting was utilized to identify the underlying pathway through which ARHGAP11A silencing mediates biological roles in LUAD. Results: ARHGAP11A was significantly over-expressed in LUAD tissues. Patients in the high ARHGAP11A expression subgroup experienced worse overall survival compared to the low expression subgroup. Univariate and multivariate analysis exhibited that ARHGAP11A was an independent prognostic predictor for LUAD. After ARHGAP11A silencing in A549 cells, cell proliferation rate, invasive and migratory capacity were observed to be inhibited. Remarkably, western blot results exhibited that reduction of ARHGAP11A remarkably inhibited the expression of ROCK, pLIMK2, and pCofilin in A549 cells. Conclusion: Increased ARHGAP11A expression could regulate LUAD cell proliferation and metastasis, and identified it as a poor prognostic biomarker in LUAD.
