DNMT3B regulates proliferation of A549 cells through the microRNA‑152‑3p/NCAM1 pathway

• Published in: Oncology letters Vol. 23; no. 1; p. 1
• Main Authors: Yang, Bo, Huang, Shiqing, Chen, Hongming, Li, Rizhu, Hou, Shihao, Zhao, Jingjing, Li, Yepeng
• Format: Journal Article
• Language: English
• Published: Athens Spandidos Publications 01-01-2022; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Apoptosis; Binding sites; Cell growth; DNA methylation; Epigenetic inheritance; Flow cytometry; Gene expression; Liver cancer; Lung cancer; Lung cancer, Non-small cell; Medical prognosis; Methylation; Methyltransferases; MicroRNA; MicroRNAs; Proteins; Sulfites; Tumors
• ISSN: 1792-1074; 1792-1082
• DOI: 10.3892/ol.2021.13129

The purpose of the present study was to examine the epigenetic mechanism by which microRNA (miR)-152-3p regulates proliferation in non-small cell lung cancer A549 cells via neural cell adhesion molecule 1 (NCAM1). Bisulfite sequencing PCR (BSP), the gold standard for methylation detection, uses bisulfte-treated DNA to determine its pattern of methylation. Treatment of DNA with bisulfite converts cy tosine residues to uracil, but leaves 5-methylcy tosine residues unaffected. It was conducted and demonstrated a relatively high level of methylation in the miR-152-3p promoter region. Chromatin immunoprecipitation was combined with PCR to detect the binding of DNA methyltransferase 3B (DNMT3B) protein to miR-152-3p, which tends to occur in the core region of the miR-152-3p gene in A549 cells. Luciferase assay identified NCAM1 as the target gene of miR-152-3p. MTT, colony formation and Transwell assays indicated that miR-152-3p could decrease cell proliferation and invasion and in addition to reducing the expression level of NCAM1. Overexpression of NCAM1 could attenuate the effect of miR-152-3p. DNMT3B knockdown decreased the proliferative ability of A549 cells and increased the expression of miR-152-3p, while decreased that of NCAM1. After treatment with miR-152-3p inhibitor, these effects were attenuated and the NCAM1 expression level was upregulated. The results indicated that miR-152-3p may suppress the proliferation of A549 cells by downregulating NCAM1. In addition, DNMT3B negatively regulated the expression of miR-152-3p via modulation of the methylation level in the miR-152-3p core region, thus mediating the proliferation of lung tumor cells.