科研之友
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摘要
OBJECTIVE: miRNA-543 has antitumor activity and it is a tumor suppressor. There is little research on the regulation of miRNA-543 and its target gene in lung cancer. In this study, we investigated whether miRNA-543 can inhibit the proliferation, migration and invasion of lung adenocarcinoma cancer cells by targeting MTA1 Protein to regulate Wnt signaling pathway. METHODS: Specimens of lung cancer tissues and adjacent tissues from 72 lung adenocarcinoma patients were selected from February 1st 2017 to August 1st 2018 in 72 patients with lung adenocarcinoma. Expression of miRNA-543 and MTA 1 was detected by using qRT-PCR method. Expression levels of MTA 1 and miRNA-543 were detected respectively in PC-9, A549 and NCI-H1299 human lung adenocarcinoma cell lines and human normal lung epithelial cells, and the cells with lowest expression level were selected as subjects, which were divided into blank control group, negative control group and miRNA-543 mimic group, respectively. CCK8 method and clonogenesis experiment were used to detect the proliferation and clonogenesis of cells in each group. The expression of Cyclin D1 was detected by Western blot and qRT-PCR. Using scratch test and Transwell invasion test to detect cell migration and invasion ability. The targeting relationship between miRNA-543 and MTA1 Protein was verified by double luciferase target experiment. The expression of MTA1 Protein, Wnt5a and β-Catenin was detected by Western blot and qRT-PCR. RESULTS: The relative expression level of miRNA-543 in lung cancer tissue (1.22±0.22) was lower than that in paracancer tissue (4.55±0.76), the difference was statistically significant (t=35.924, P<0.05); while the relative expression level of MTA1 in lung cancer tissue (1.66±0.29) was higher than that in paracancer tissue (0.77±0.24), the difference was statistically significant (t=20.096, P<0.05), and there was a negative correlation between them in lung tissue (r=-0.387, P=0.001). The expression level of miRNA-543 in human lung cancer cell lines was lower than that in human normal lung epithelial cells (F=46.784, P<0.05), and the lowest in A549 cell lines. After overexpression of miRNA-543, the proliferation ability of A549 cells in 48, 72 and 96 h was lower than that in the blank control group and miRNA-543 mimic NC group (all P<0.05), and the ability of cell clone formation, cell migration and invasion were all reduced (all P<0.05). The results of luciferase report showed that MTA1 was the target gene of miRNA-543, and the expression levels of MTA1, Wnt5a, β-Catenin protein and mRNA in miRNA-543 mimic group were all decreased (all P<0.05). CONCLUSION: miRNA-543 can inhibit the proliferation, migration and invasion of A549 cells by targeting the expression of MTA1, which may play a role by inhibiting the activation of Wnt/β-catenin signaling pathway.
