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MiR-326 mediates malignant biological behaviors of lung adenocarcinoma by targeting ZEB1.

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机构: [1]School of medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China [2]Integrative Cancer Center & Cancer Clinical Research Center, Sichuan Cancer Hospital & Institute Sichuan, Cancer Center, School of Medicine University, Sichuan, China [3]The General Hospital of Western Theater Command, Chengdu, Sichuan, China [4]Guangxi Medical University, Nanning, Guangxi, P.R. China
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关键词: Lung adenocarcinoma miR-326 malignant biological behaviors zinc-finger-enhancer binding protein 1 epithelial mesenchymal transition

摘要:
MiR-326 functions as an antioncogene in the several types of cancer. However, the underling mechanisms through which miRNA-326 regulates the anti-carcinogenesis of lung adenocarcinoma have remained elusive. The aim of this study was to explore the role and regulatory mechanism of miR-326 in cell proliferation, invasion, migration and apoptosis in lung adenocarcinoma. Quantitative real-time PCR (qRT-PCR) was used to detect the expression pattern of miR-326 in human bronchial epithelial cells (HBES-2B), 4 kinds of lung adenocarcinoma cell lines (H23, H1975, H2228, H2085) and 20 lung adenocarcinoma tissues. Then, H23 cells were infected with miR-326 mimics, miR-326 inhibitors and si-ZEB1 to build up-regulated miR-326 cell lines, down-regulated ZEB1(zinc-finger-enhancer binding protein 1)cell lines, simultaneous down-regulated ZEB1 and miR-326 cell lines. Moreover, CCK-8 assay, transwell invasion assay, wound healing assay and flow cytometry assay were employed to examine the effects of miR-326 and ZEB1 on the proliferation, invasion, migration and apoptosis abilities of H23 cells. Western blot was performed to explore the effects of miR-326 and ZEB1 on the expression of invasion and migration related proteins N-cadherin, E-cadherin, MMP7, MMP13, SLUG and apoptotic proteins PARP, BAX. On the mechanism, a dual-luciferase reporter gene was used to measure the target relationship between miR-326 and ZEB1. MiR-326 expression was significantly downregulated in lung adenocarcinoma tissues and cells. Overexpression of miR-326 significantly inhibited the malignant behaviors of H23 cells. Mechanically, luciferase reporter assay showed that ZEB1 was a direct target of miR-326. MiR-326 mimic downregulated the expression of ZEB1. Furthermore, knocking down ZEB1 strongly inhibited the proliferation, invasion and migration of H23 cells but promoted apoptosis. MiR-326 could target ZEB1 to inhibit the proliferation, invasion and migration of lung adenocarcinoma cells and promote apoptosis, which is a potential therapeutic target for lung adenocarcinoma.

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出版当年[2021]版:
大类 | 4 区 综合性期刊
小类 | 4 区 综合性期刊
最新[2023]版:
大类 | 4 区 综合性期刊
小类 | 4 区 综合性期刊
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第一作者机构: [1]School of medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China [2]Integrative Cancer Center & Cancer Clinical Research Center, Sichuan Cancer Hospital & Institute Sichuan, Cancer Center, School of Medicine University, Sichuan, China
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通讯机构: [1]School of medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China [*1]School of Medicine, University of Electronic Science and Technology of China, No. 4, Section 2, Jianshe North Road, Chenghua District, Chengdu, Sichuan 610000, P.R. China
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