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August 18, 2025BMC CancerOpen Access

METTL16-dependent GPX4 m6A modification links ferroptosis to NSCLC TKIs resistance

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Authors

YZYingou ZengQWQiang WangDQDi Qiao

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Implication

Analysis shows METTL16 enhances GPX4 m6A modification in NSCLC cells, suggesting a link to TKI resistance.

Key Points

  • METTL16 increases GPX4 m6A modification, which promotes NSCLC proliferation and resistance to AZD-9291.
  • Upregulation of METTL16 correlates with worse prognosis in NSCLC, highlighting its role in cancer progression.
  • Observational analysis across datasets revealed GPX4 as a target of METTL16, influencing ferroptosis regulation.
  • Targeting METTL16 may enhance sensitivity to AZD-9291, presenting a novel therapeutic strategy for NSCLC.

Cite This Study

Zeng et al. (2025) studied this question.

synapsesocial.com/papers/68af2d83cf1dd9ea359e5db1https://doi.org/10.1186/s12885-025-14729-1
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