MiR-129-2-3p Inhibits Esophageal Carcinoma Cell Proliferation, Migration, and Invasion via Targeting DNMT3B

Abstract

Purpose: The study aims to explore the regulatory mechanism of miR-129-2-3p underly-ing esophageal carcinoma (EC) cell progression and generate new ideas for targeted treatment of EC. Methods: Mature miRNA expression data and total RNA sequencing data of EC in the TCGA-ESCA dataset were utilized to explore differentially expressed miRNAs (DEmiRNAs). StarBase da-tabase was then utilized to predict targets of miRNA. MiR-129-2-3p and DNMT3B expression in EC cell lines was assayed through qRT-PCR and Western blot. CCK-8, scratch healing, and transwell assays were conducted to assess the impact of miR-129-2-3p on EC cell phenotypes. In addition, a dual-luciferase assay was completed to identify the binding relationship between DNMT3B and miR-129-2-3p. Results: MiR-129-2-3p was noticeably less expressed in EC cell lines, while DNMT3B was highly expressed. MiR-129-2-3p could bind to DNMT3B. Furthermore, in vitro functional experiments un-covered that overexpressed miR-129-2-3p repressed EC cell progression while further overexpress-ing DNMT3B would restore the above inhibitory effect. Conclution: MiR-129-2-3p is a cancer repressor in EC cells, and it could target DNMT3B, thus hampering the progression of EC cells.