METTL3‑mediated m6A modification of Bcl‑2 mRNA promotes non‑small cell lung cancer progression
- Yongxi Zhang
- Shuyuan Liu
- Tiesuo Zhao
- Chengxue Dang
Affiliations: Department of Oncology, The First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China, Department of Oncology, The Third Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China, Department of Immunology, Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China
- Published online on: June 15, 2021 https://doi.org/10.3892/or.2021.8114
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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 in vitro and, as well as tumorigenicity in vivo. 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 in vivo and in vitro. 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.