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FTO-mediated the destabilization of RASGRF1 mRNA impedes thyroid cancer progression and suppresses macrophage M2

Zongyu Li1, Jiancang Ma1, Hao Guan1

  • 1Department of Vascular Surgery, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, Shaanxi, China.

Cell Biology and Toxicology
|August 5, 2025
PubMed
Abstract

Insights

RASGRF1 promotes thyroid cancer (THCA) progression by stabilizing its mRNA. Inhibiting RASGRF1 or upregulating FTO reduces cancer growth and M2 macrophage polarization, offering potential THCA treatment strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • RASGRF1 is implicated in various human cancers, including thyroid cancer (THCA).
  • Understanding RASGRF1's role and its regulatory mechanisms in THCA is crucial for developing targeted therapies.

Purpose of the Study:

  • To define the activity of RASGRF1 in THCA progression.
  • To elucidate the m6A modification mechanism governing RASGRF1 dysregulation in THCA.

Main Methods:

  • Expression analysis (immunoblotting, IHC, qPCR).
  • Cell proliferation, apoptosis, invasion, and migration assays.
  • In vivo xenograft studies and macrophage polarization analysis.
  • RNA immunoprecipitation (RIP) and methylated RNA immunoprecipitation (MeRIP) assays to assess FTO's influence on RASGRF1 mRNA.

Main Results:

  • RASGRF1 is upregulated in THCA and promotes tumor growth, metastasis, and M2 macrophage polarization.
  • FTO reduces RASGRF1 mRNA stability through an m6A-dependent mechanism.
  • FTO upregulation suppresses THCA progression by downregulating RASGRF1, inhibiting M2 macrophage polarization and migration.

Conclusions:

  • FTO-mediated RASGRF1 mRNA instability inhibits THCA progression and M2 macrophage polarization.
  • Targeting RASGRF1 presents a potential therapeutic strategy for THCA treatment.
Keywords:
FerroptosisM6A modificationMacrophage M2 polarizationRASGRF1Thyroid cancer

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