METTL3‑mediated m6A modification of Bcl‑2 mRNA promotes non‑small cell lung cancer progression.

Oncol Rep

Department of Oncology, The First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.

Published: August 2021

AI Article Synopsis

  • - Methyltransferase-like 3 (METTL3) modifies RNA by adding a methyl group (m6A), playing a significant role as an oncogene in various cancers, including non-small cell lung cancer (NSCLC), where its function is still not well understood.
  • - The study found that METTL3 is overexpressed in NSCLC tissues, and manipulating its levels (either increasing or decreasing) directly impacts NSCLC cell viability, migration, and apoptosis.
  • - METTL3 enhances the translation of Bcl-2, a protein that promotes cell survival, through m6A modification, suggesting that targeting METTL3 could provide a new strategy for NSCLC treatment.

Article Abstract

Methyltransferase‑like 3 (METTL3) is an RNA methyltransferase that mediates modification of N6‑methyladenosine (m6A), which serves as an oncogene in various types of cancer. The role of m6A modification in the onset and progression of cancer has attracted growing attention. However, the functional and regulatory mechanisms of METTL3 in non‑small cell lung cancer (NSCLC) progression are still poorly understood. In the present study, METTL3 expression in NSCLC tissue was analyzed using the Gene Expression Profiling Interactive Analysis database. Western blotting and reverse transcription‑quantitative PCR were performed to evaluate the expression of METTL3 in NSCLC tissue and cell lines. Here, knockdown and overexpression of METTL3 notably decreased NSCLC cell viability, apoptosis and migration and, as well as tumorigenicity . Expression of METTL3 was upregulated in NSCLC tissue. METTL3 overexpression promoted cell viability and migration in NSCLC, while knockdown of METTL3 yielded the opposite result and . METTL3 increased Bcl‑2 translation via m6A modification, which increased viability and enhanced migration of NSCLC cells. METTL3 served as an oncogene in NSCLC via METTL3‑mediated Bcl‑2 mRNA m6A modification, which indicated that targeting METTL3 may be an effective therapeutic strategy for clinical management of NSCLC.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8218297PMC
http://dx.doi.org/10.3892/or.2021.8114DOI Listing

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