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

Abstract

Purpose: To explore regulatory mechanism of miR-129-2-3p underlying 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 TCGA-ESCA dataset were utilized to explore differentially expressed miRNAs (DEmiRNAs). StarBase database was then utilized to predict targets of miRNA. MiR-129-2-3p and DNMT3B expression in EC cell lineswas 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, dual-luciferase assay was completed to identify binding relationship between DNMT3B and miR-129-2-3p. Results: MiR-129-2-3p was noticeably less expressed in EC tissue, while DNMT3B was highly expressed. MiR-129-2-3p could bind to DNMT3B. Furthermore, in vitro functional experiments uncovered that overexpressed miR-129-2-3p repressed EC cell dysregulation of is often confirmed in solid tumors. Xiao Y et al.[18] discovered that miR-129-2 affects invasion and proliferation of lung cancer cells. Similarly, Wang D et al.[19] found that miR-129-1-3p constrains gastric cancer cell migration via modulating BDKRB2. However, there has been no research reported on the impact of miR-129-2-3p on EC. Conclution: MiR-129-2-3p is a cancer repressor in EC cells, and it could target DNMT3B, thus hampering progression of EC cells.

Prognostic and therapeutic potential of microRNAs for fracture healing processes and non‐union fractures: A systematic review

“…Twenty‐four studies analysed miRNAs in blood or tissue samples (bone biopsies) of fracture patients 45,54–76 . Blood or tissue samples were collected during surgery, subsequently RNA was extracted, and validation of miRNAs was performed.…”

“…45, Blood or tissue samples were collected during surgery, subsequently RNA was extracted, and validation of miRNAs was performed. In detail, n = 18 studies 45,[55][56][57][59][60][61][62][63][65][66][67][68][69][70][71]74,76 analysed blood samples and n = 11 studies 45,54,55,[64][65][66][67]72,73,75,76 analysed samples collected from bone biopsies. Five studies 45,54,55,65,67 analysed both blood and tissue samples.…”

“…Five studies 45,54,55,65,67 analysed both blood and tissue samples. Twenty studies [54][55][56][57][58][59][60][61][62][63][64][65][66][67][68][69][73][74][75][76] validated their findings from clinical screening in an in vitro model, eight studies 54,64,65,67,69,73,75,76 used an animal model for validation, and all of the studies investigating an animal model for validation also performed additional in vitro validation.…”

Comprehensive analysis of m6A/m5C/m1A-related gene expression, immune infiltration, and sensitivity of antineoplastic drugs in glioma

“…Glioma growth is slowed in vitro and in vivo experiments when a DNMT1 inhibitor is given ( 36 ). Currently, there is no specific research on DNMT3B in glioma, but DNMT3B has been reported to accelerate the occurrence and progression of esophageal cancer ( 38 ), lung cancer ( 39 ), breast cancer ( 40 ), and ovarian cancer ( 41 ), implying that DNMT3B is an essential biomarker in cancer pathogenesis.…”

Non-coding RNAs/DNMT3B axis in human cancers: from pathogenesis to clinical significance

“…Interestingly, their findings also indicated that the inhibitory effect could be counteracted by the additional overexpression of DNMT3B. In this manner, miR-129-2-3p acts as a tumor suppressor in EC cells by targeting and inhibiting DNMT3B [ 26 ].…”