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Abstract <p>Lung cancer continues to be the leading reason for deaths related to cancer worldwide, with non-small cell lung cancer (NSCLC) accounting for almost 85% of all cases. Extensive evidence suggests that the involvement of N6-methyladenosine (m6A) is crucial in the advancement of NSCLC, emphasizing the need for additional research into its functions and mechanisms. The purpose of this research was to explore the function of METTL3 in NSCLC by examining its involvement in m6A RNA methylation and FBXO33 degradation. The study utilized bioinformatics analysis of TCGA data, methylation-specific PCR (MSP), RT-qPCR, Western blotting, CCK-8, Edu, and flow cytometry assays to examine the role of METTL3 and FBXO33 in NSCLC. In vivo, tumorigenesis experiments were conducted using nude mice. Bioinformatics analysis demonstrated a notable inverse correlation between FBXO33 methylation levels and mRNA expression in NSCLC tissues. METTL3 was observed to be upregulated in NSCLC cells, enhancing m6A methylation of FBXO33, which resulted in its degradation. Silencing METTL3 reduced NSCLC cell proliferation and viability while promoting apoptosis. These effects were partially reversed by co-silencing FBXO33. In vivo experiments confirmed that silencing METTL3 suppressed tumor growth, partially dependent on FBXO33. METTL3 promotes NSCLC progression by modulating m6A methylation of FBXO33, influencing cell proliferation, viability, and apoptosis. These results suggest that focusing on METTL3 and FBXO33 could be a beneficial treatment strategy for advanced NSCLC. More investigation is required to uncover more targets of METTL3-induced m6A modification and investigate its potential clinical uses in treating NSCLC.</p>

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METTL3 Contributes to the Advancement of Non-Small Cell Lung Cancer by Regulating m6A RNA Methylation-Mediated Degradation of FBXO33

  • 期刊论文

  • 发表日期：

    2025年12月1日

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  • Q. Wei,
  • S. Lin,
  • W. Jiang,
  • H. Xie,
  • Z. Lin,
  • K. Wang,
  • H. He

摘要

Abstract

Lung cancer continues to be the leading reason for deaths related to cancer worldwide, with non-small cell lung cancer (NSCLC) accounting for almost 85% of all cases. Extensive evidence suggests that the involvement of N6-methyladenosine (m6A) is crucial in the advancement of NSCLC, emphasizing the need for additional research into its functions and mechanisms. The purpose of this research was to explore the function of METTL3 in NSCLC by examining its involvement in m6A RNA methylation and FBXO33 degradation. The study utilized bioinformatics analysis of TCGA data, methylation-specific PCR (MSP), RT-qPCR, Western blotting, CCK-8, Edu, and flow cytometry assays to examine the role of METTL3 and FBXO33 in NSCLC. In vivo, tumorigenesis experiments were conducted using nude mice. Bioinformatics analysis demonstrated a notable inverse correlation between FBXO33 methylation levels and mRNA expression in NSCLC tissues. METTL3 was observed to be upregulated in NSCLC cells, enhancing m6A methylation of FBXO33, which resulted in its degradation. Silencing METTL3 reduced NSCLC cell proliferation and viability while promoting apoptosis. These effects were partially reversed by co-silencing FBXO33. In vivo experiments confirmed that silencing METTL3 suppressed tumor growth, partially dependent on FBXO33. METTL3 promotes NSCLC progression by modulating m6A methylation of FBXO33, influencing cell proliferation, viability, and apoptosis. These results suggest that focusing on METTL3 and FBXO33 could be a beneficial treatment strategy for advanced NSCLC. More investigation is required to uncover more targets of METTL3-induced m6A modification and investigate its potential clinical uses in treating NSCLC.