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August 4, 2025

Supplementary Figure S1 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

Experimental findings demonstrate METTL3's role in gastric cancer signaling, implicating FNTA and ERK activation in epithelial cells.

Key Points

  • MAIN FINDING: METTL3 promotes gastric cancer progression, indicating its potential as a therapeutic target.
  • KEY EVIDENCE: METTL3 deficiency alters FNTA signaling, which affects KRAS/ERK pathways in gastric cells.
  • APPROACH: Analysis was conducted on human normal gastric mucosal epithelial cells to assess METTL3's role.
  • SIGNIFICANCE: Understanding METTL3's impact could lead to new strategies for treating gastric cancer effectively.

Cite This Study

Hu et al. (2025) studied this question.

synapsesocial.com/papers/689a0f86e6551bb0af8d0980https://doi.org/10.1158/1541-7786.29819563
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Also Consider

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

  1. 1Supplementary Figure S3 from METTL3 Promotes Gastric Cancer Progression via Modulation of FNTA-Mediated KRAS/ERK Signaling Activation2025
  2. 2Supplementary Figure S2 from METTL3 Promotes Gastric Cancer Progression via Modulation of FNTA-Mediated KRAS/ERK Signaling Activation2025
  3. 3Data from METTL3 Promotes Gastric Cancer Progression via Modulation of FNTA-Mediated KRAS/ERK Signaling Activation2025
  4. 4Supplementary Figure S9 from TERC Stimulates Fatty Acid Metabolism to Promote Bladder Cancer Progression2025
  5. 5METTL3-Regulated lncRNA SNHG7 Drives MNNG-Induced Epithelial–Mesenchymal Transition in Gastric Precancerous Lesions2024 · 10 citations