miR-212-5p inhibits nasopharyngeal carcinoma progression by targeting METTL3

Abstract

This study was conducted to investigate the effect of microRNA-212-5p (miR-212-5p) on the proliferation and apoptosis of nasopharyngeal carcinoma (NPC) cells. Microarray datasets (EXP00394 and EXP00660) were downloaded from the dbDEMC database, and the differentially expressed microRNAs between high-grade and low-grade NPC were analyzed. miR-212-5p and methyltransferase like 3 (METTL3) expression levels in NPC tissues and cells were determined by the quantitative real-time polymerase chain reaction and Western blot. Besides, the relationship between miR-212-5p expression and clinicopathological characteristics of patients was analyzed by the Chi-square test. Cell counting kit-8 assay, 5-ethynyl-2-deoxyuridine (EdU) assay, and flow cytometry were adopted to detect the effect of miR-212-5p on the cell proliferation and apoptosis. Kyoto Encyclopedia of Genes and Genomes and Gene Ontology analysis were performed to explore the potential biological functions and the signal pathways related to the target genes of miR-212-5p. Bioinformatics prediction and dual luciferase reporter gene assay were used to verify the relationship between miR-212-5p and METTL3 3′ untranslated region. Besides, western blot was adopted to detect the expression of METTL3. Gene set enrichment analysis was performed to analyze the downstream pathways in which METTL3 was enriched. It was found that miR-212-5p was downregulated in NPC tissues, and the low miR-212-5p expression was associated with lymph node metastasis and poor differentiation. miR-212-5p overexpression inhibited the growth and promoted apoptosis of NPC cells; miR-212-5p inhibition functioned oppositely. Mechanistically, miR-212-5p inhibited the proliferation and promoted apoptosis of NPC cells via suppressing METTL3 expression. miR-212-5p/METTL3 was associated with processes of RNA transport and cell cycle. In conclusion, miR-212-5p inhibits the progression of NPC by targeting METTL3.

MicroRNA miR-212-5p Regulates the MEK/ERK Signaling Pathway by Targeting A-Raf proto-oncogene serine/threonine-protein kinase (ARAF) to Regulate Cowshed PM2.5-Induced NR8383 Apoptosis

“…This has become strong epiphenomenal evidence in this article to understand the process of apoptosis caused by cowshed PM 2.5 . It is undeniable that miR-212-5p regulates multiple target genes, which have the same or different functions [ 32 , 46 , 47 ], all of which suggest that miR-212-5p has complex biological functions depending on the target genes and cellular context. Some articles have reported that miR-212-5p can regulate some physiological activities, such as cell proliferation and epithelial mesenchymal transition [ 48 , 49 ], but the regulation of apoptosis after cowshed PM 2.5 stimulation by miR-212-5p has not been reported.…”

LINC00599 influences smoke-related chronic obstructive pulmonary disease and regulates CSE-induced epithelial cell apoptosis and inflammation by targeting miR-212-5p/BASP1 axis

“…26 In our investigation, based on bioinformatics analysis, miR-212-5p was screened and verified to bind with LINC00599 in 16HBE cells. As an important member of the miR family, miR-212-5p has been reported to be dysregulated in a variety of human diseases, such as non-alcoholic fatty liver disease, 27 nasopharyngeal carcinoma, 28 and ovarian cancer. 29 For example, circ_0,099630 curbed periodontal ligament cells proliferation and osteogenic differentiation through elevating SPRY1 expression via sponging miR-212-5p in periodontitis.…”