Decreased miR-124 contributes to the epithelial-mesenchymal transition phenotype formation of lung adenocarcinoma cells via targeting enhancer of zeste homolog 2.

INTRODUCTION:MiR-124, a tumor suppressor, is involved in regulating various cellular processes. The purpose of this study was to investigate the possible function of miR-124 in LA (lung adenocarcinoma) cells. AIMS:MiR-124 expression levels in the 54 pairs of LA tissues (and corresponding non-tumor tissues) obtained at the Sixth People's Hospital of Yancheng City and in LA cells were assessed by qRT-PCR. Colony formation assay, wound healing assay, transwell assays, attachment/detachment, western blotting and immunofluorescence assays were performed to assess the function of miR-124 on proliferation, migration and epithelial-to-mesenchymal (EMT) phenotypes in LA cells in vitro. Enhancer of zeste homolog 2 (EZH2) is identified as a target of miR-124 by bioinformatics analysis and luciferase reporter assays. Rescue assays were applied to verify the relationship between miR-124 and EZH2. RESULTS:MiR-124 was down-regulated in LA tissues (compared to adjacent non-tumor tissues), and was down-regulated in 3 out of 4 lung cancer cell lines compared to immortalized, non-tumorigenic bronchial epithelial cells. Forced expression of miR-124 significantly suppressed tumor cell proliferation, migration and inhibited the EMT process. On the contrary, deletion of miR-124 could obviously promote cell proliferation, migration and facilitate the formation of EMT phenotype. Bioinformatics analysis and luciferase reporter assays confirmed that EZH2 was a target gene of miR-124 and was negatively correlated with the level of miR-124 in cancer tissues. CONCLUSION:Our current study suggested that miR-124 was a tumor suppressor in LA, and miR-124 was associated with LA cell EMT phenotype formation via targeting EZH2.

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