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METTL3 promotes ovarian cancer progression through YTHDF2-dependent degradation of GATA4

Di Zhao1, Mengya Li2, Peiling Li1

  • 1Department of Gynecology and Obstetrics, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.

Pathology, Research and Practice
|September 13, 2025
PubMed

Insights

METTL3 promotes ovarian cancer (OC) by degrading the tumor suppressor GATA4. Inhibiting METTL3 restores GATA4, reducing OC malignancy and offering new therapeutic strategies.

Area of Science:

  • Oncology
  • Epigenetics
  • RNA Biology

Background:

  • Ovarian cancer (OC) is a lethal gynecological malignancy with poor therapeutic outcomes.
  • N6-methyladenosine (m6A) RNA modification is implicated in tumorigenesis, but its role in OC requires elucidation.

Purpose of the Study:

  • To investigate the role of METTL3 in OC progression.
  • To elucidate the molecular mechanisms by which METTL3 influences OC development.

Main Methods:

  • Investigated the interaction between METTL3, YTHDF2, and GATA4 in OC cells.
  • Utilized pharmacological inhibition of METTL3 (STM2457) and single-cell RNA sequencing (scRNA-seq).

Main Results:

  • METTL3 promotes OC progression by mediating GATA4 mRNA degradation via YTHDF2.
  • METTL3-induced GATA4 suppression is linked to aberrant EMT, proliferation, and stromal remodeling in the OC microenvironment.
  • Pharmacological inhibition of METTL3 increased GATA4 levels and attenuated OC phenotypes.

Conclusions:

  • A novel METTL3-YTHDF2 regulatory axis destabilizes GATA4 mRNA, driving OC progression.
  • Targeting this axis presents a potential therapeutic strategy for ovarian cancer.
Keywords:
GATA4METTL3Ovarian cancerYTHDF2

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