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August 4, 2025

Data from METTL3 Promotes Gastric Cancer Progression via Modulation of FNTA-Mediated KRAS/ERK Signaling Activation

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Authors

FHFangqi HuSZSong ZhangJCJie Chai

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Overview

Research reveals METTL3 boosts gastric cancer progression via FNTA, suggesting a new therapeutic target for treatment.

Key Points

  • PNETTL3 plays a crucial role in gastric cancer progression through RNA methylation.
  • Higher METTL3 correlates with poor patient outcomes in gastric cancer cases.
  • Silencing METTL3 or FNTA disrupts KRAS signaling, inhibiting cancer growth in various settings.
  • Targeting the METTL3/FNTA pathway may help combat resistance to existing KRAS inhibitors.

Cite This Study

Hu et al. (2025) studied this question.

synapsesocial.com/papers/689a0f86e6551bb0af8d0971https://doi.org/10.1158/1541-7786.c.7963852
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1METTL3-mediated N6-methyladenosine modification of STAT5A promotes gastric cancer progression through regulating KLF42024
  2. 2Supplementary Figure S3 from METTL3 Promotes Gastric Cancer Progression via Modulation of FNTA-Mediated KRAS/ERK Signaling Activation2025
  3. 3Supplementary Figure S1 from METTL3 Promotes Gastric Cancer Progression via Modulation of FNTA-Mediated KRAS/ERK Signaling Activation2025
  4. 4Supplementary Figure S2 from METTL3 Promotes Gastric Cancer Progression via Modulation of FNTA-Mediated KRAS/ERK Signaling Activation2025
  5. 5METTL3-mediated N6-methyladenosine modification of STAT5A promotes gastric cancer progression by regulating KLF42024 · 15 citations