ArticleThoracic cancer2024
METTL3/IGF2BP1 influences the development of non-small-cell lung cancer by mediating m6A methylation modification of TRPV1.
Article in Thoracic cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Dihydrocapsaicin suppresses the migration and invasion of gastric cancer cells by upregulating TRPV1 expression.In vitro cellular & developmental biology. Animal · 2026Article
- TRPV1 Downregulation Impairs Prostate Cancer Growth: Functional and Translational Insights from Cellular andInternational journal of biological sciences · 2026Article
- The role of m6A modification in non-small cell lung cancer: functional insights and impact on therapy resistance.Cancer cell international · 2025Review
- The m6A methyltransferase METTL3 affects ferroptosis in non-small cell lung cancer by regulating the PTEN/PI3K/AKT pathway.Discover oncology · 2025Article
- Abnormal expression of CDC25C in NSCLC is influenced by transcriptional and RNA N6‑methyladenosine‑mediated post‑transcriptional regulation.International journal of oncology · 2025Article
- Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) in hematological diseases.Molecular medicine (Cambridge, Mass.) · 2024Review
- METTL3/IGF2BP1 influences the development of non-small-cell lung cancer by mediating m6A methylation modification of TRPV1.Thoracic cancer · 2024Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundMethyltransferase 3 (METTL3) accelerates N6-methyladenosine (m6A) modifications and affects cancer progression, including non-small-cell lung cancer (NSCLC). In this study, we aimed to explore the regulatory mechanisms of METTL3 underling NSCLC.
methodsImmunohistochemical assay, quantitative real-time polymerase chain reaction (qRT-PCR) assay, and western blot assay were conducted for gene expression. MTT assay and colony formation assay were performed to explore cell proliferation capacity. Cell apoptosis and THP-1 cell polarization were estimated by flow cytometry analysis. Cell migration and invasion capacities were evaluated by transwell assay. Methylated RNA immunoprecipitation assay, dual-luciferase reporter assay, actinomycin D treatment and RIP assay were performed to analyze the relationships of METTL3, insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1), and transient receptor potential cation channel subfamily V member 1 (TRPV1). The functions of METTL3 and TRPV1 in vivo were investigated through establishing the murine xenograft model.
resultsTRPV1 expression was upregulated in NSCLC and related poor prognosis. TRPV1 silencing inhibited NSCLC cell growth and metastasis, induced NSCLC cell apoptosis, and repressed M2 macrophage polarization. The results showed that METTL3 and IGF2BP1 could regulate TRPV1 expression through m6A methylation modification. Moreover, METTL3 deficiency inhibited NSCLC cell growth, metastasis, and M2 macrophage polarization and facilitated NSCLC cell apoptosis, while TRPV1 overexpression restored the impacts. In addition, METTL3 knockdown restrained tumor growth in vivo via regulating TRPV1 expression.
conclusionMETTL3 bound to IGF2BP1 and enhanced IGF2BP1's m6A recognition of TRPV1 mRNA, thereby promoting NSCLC cell growth and metastasis, and inhibiting M2 macrophage polarization.
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