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.

MiR-326 在多种类型的癌症中充当抑癌基因。然而，miRNA-326 调节肺腺癌抗癌作用的基本机制仍不清楚。本研究旨在探讨miR-326在肺腺癌细胞增殖、侵袭、迁移和凋亡中的作用及调控机制。采用实时定量PCR（qRT-PCR）检测miR-326在人支气管上皮细胞（HBES-2B）、4种肺腺癌细胞系（H23、H1975、H2228、H2085）和20种细胞中的表达模式。肺腺癌组织。然后，用miR-326模拟物、miR-326抑制剂和si-ZEB1感染H23细胞，构建上调miR-326细胞系、下调ZEB1（锌指增强剂结合蛋白1）细胞系，同时下调-调节ZEB1和miR-326细胞系。此外，采用CCK-8实验、Transwell侵袭实验、伤口愈合实验和流式细胞仪实验检测miR-326和ZEB1对H23细胞增殖、侵袭、迁移和凋亡能力的影响。通过Western blot检测miR-326和ZEB1对侵袭迁移相关蛋白N-cadherin、E-cadherin、MMP7、MMP13、SLUG以及凋亡蛋白PARP、BAX表达的影响。在机制上，使用双荧光素酶报告基因来测量miR-326和ZEB1之间的靶关系。miR-326 表达在肺腺癌组织和细胞中显着下调。miR-326的过表达显着抑制H23细胞的恶性行为。从机械角度来看，荧光素酶报告基因检测显示 ZEB1 是 miR-326 的直接靶标。MiR-326 模拟物下调 ZEB1 的表达。此外，敲低ZEB1强烈抑制H23细胞的增殖、侵袭和迁移，但促进细胞凋亡。MiR-326可以靶向ZEB1抑制肺腺癌细胞的增殖、侵袭和迁移并促进细胞凋亡，是肺腺癌的潜在治疗靶点。