ArticleBMC cancer2025
METTL16-dependent GPX4 m
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- RNA modifications as determinants of cancer cell death: from epitranscriptomic mechanisms to therapeutic targeting.Functional & integrative genomics · 2026Review
- USP20 governs tyrosine kinase inhibitors resistance through ferroptosis evasion by targeting GPX4 in cancers.Redox biology · 2026Article
- Mechanism and therapeutic prospects of ferroptosis regulation through m6A in cancer.Frontiers in cell and developmental biology · 2026Review
- Targeting ferroptosis in lung cancer: pharmacological regulation, nanomedicine-based delivery, and AI-enabled translational strategies.American journal of cancer research · 2026Review
- METTL16 emerges as a pivotal epitranscriptomic regulator, linking RNA modification, tumor progression, and immune modulation.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundNon-small-cell lung cancer (NSCLC) is a highly aggressive cancer with a poor prognosis, largely due to increasing resistance to Tyrosine Kinase Inhibitors (TKIs). The mechanisms of NSCLC TKI resistance remain unknown. This study aimed to elucidate the molecular mechanism of METTL16-mediated GPX4 m
methodsTCGA, and GEO datasets were used to analyze the differential expression of m
resultsMETTL16 was significantly upregulated in NSCLC tissue and was associated with a worse prognosis. Overexpression of METTL16 significantly promoted the proliferation and AZD-9291 resistance of NSCLC, while METTL16 knockdown inhibited the above phenotype. Through bioinformatic analysis and experimental results, we found that GPX4 mRNA is a substrate of METTL16. GPX4 was upregulated in AZD-9291-resistant NSCLC cells and ferroptosis was inhibited. As a key regulator of ferroptosis, METTL16 mediated GPX4 m
conclusionsIn summary, we found that METTL16-mediated GPX4 modification promoted the proliferation and AZD-9291 resistance of NSLCL by inhibiting ferroptosis activity. Our study is expected to provide a novel insight and potential therapeutic target for NSCLC AZD-9291 resistance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.