ArticleDiscover oncology2025
The m6A methyltransferase METTL3 affects ferroptosis in non-small cell lung cancer by regulating the PTEN/PI3K/AKT pathway.
Article in Discover oncology, 2025. 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.
- RNA modifications as determinants of cancer cell death: from epitranscriptomic mechanisms to therapeutic targeting.Functional & integrative genomics · 2026Review
- ARID3A knockdown facilitates ferroptosis partly through modulation of the PTEN/Akt pathway in breast cancer.Oncology letters · 2026Article
- The mechanism of deubiquitinase USP14 modifying HSP90AA1 to activate NRF2 signaling in lung cancer cell resistance to ferroptosis.Molecular biology reports · 2026Article
- Characterization of Circ_0048766: an oncogenic circular rna promoting triple-negative breast cancer progression via the miR-329-3p/CXCR4 axis and regulated by METTL3.Cancer cell international · 2026Article
- LINC00886 inhibits the proliferation, migration, and invasion of NSCLC cells by sponging miR-141-5p.Discover oncology · 2026Article
- RNA modifications and cancer ferroptosis.Cancer cell international · 2026Review
- Emerging functions of m6A-modified circRNAs and their targeting strategies in lung cancer.Frontiers in cell and developmental biology · 2026Review
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6 authors.
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Abstract
backgroundNon-small cell lung cancer (NSCLC) poses a major threat to human health, METTL3 has been reported to promote numerous tumor development by inhibiting ferroptosis. The aim of the present study was to explore the mechanism of action of METTL3 in NSCLC.
methodsThe UALCAN online platform was applied to analyze METTL3 and PTEN expression in NSCLC and their relationship with tumor stages. NCI-H23 and NCI-H1975 cells were transfected with sh-METTL3, or oe-METTL3 respectively. Then EdU assay was employed to assess cell proliferation and the transwell assay was employed to assess the ability of cells to migrate and invade. Apoptosis was detected using flow cytometry. In addition, m6A methylation levels, oxidative stress indicators, and Fe
resultsMETTL3 expression was up-regulated in NSCLC and was closely related to the tumor stages. METTL3 overexpression significantly promoted the malignant phenotype of NSCLC cells, increased the methylation level of m6A mRNA, reduced oxidative stress, inhibited the occurrence of ferroptosis and apoptosis, and led to increased expression of GPX4 and activation of the PTEN/PI3K/AKT pathway. Conversely, METTL3 knockdown produced the opposite effect. Importantly, METTL3 knockdown-induced oxidative stress and ferroptosis in NCI-H23 cells were rescued by sh-PTEN or ferroptosis inhibitor Ferrostatin-1.
conclusionMETTL3 may inhibit ferroptosis in NSCLC by activating the PTEN/PI3K/AKT pathway, suggesting that METTL3-mediated PTEN/PI3K/AKT pathway may be a promising therapeutic target for NSCLC.
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