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METTL3 stabilizes DDX17 mRNA via IGF2BP2-mediated m6A modification to suppress endometrial cancer progression

Yuan Zhang1, Mengjun Liu1, Jing Liu1

  • 1Department of Gynecologic Oncology, First Affiliated Hospital of Bengbu Medical University, No.287 Changhuai Road, Bengbu City, 233004, Anhui Province, China.

Clinical and Experimental Medicine
|August 7, 2025
PubMed
Abstract

Insights

DEAD-box helicase 17 (DDX17) suppresses endometrial cancer (EC) by stabilizing its mRNA via METTL3-mediated modification. This mechanism inhibits tumor growth and spread by inactivating the PI3K/AKT pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Endometrial cancer (EC) incidence is rising globally, with metastatic or recurrent cases having poor prognoses.
  • Novel therapeutic targets are crucial for managing advanced EC.
  • DEAD-box helicase 17 (DDX17) is a potential player in various cancers.

Purpose of the Study:

  • To investigate the biological role of DDX17 in endometrial cancer.
  • To elucidate the molecular mechanisms underlying DDX17's function in EC.
  • To explore DDX17 as a potential therapeutic target for EC.

Main Methods:

  • Analysis of DDX17 expression in EC tissues and cell lines.
  • In vitro functional assays (proliferation, migration, invasion) following DDX17 manipulation.
  • In vivo xenograft models for assessing tumor growth.
  • Mechanistic studies including RNA immunoprecipitation and m6A modification analysis.

Main Results:

  • DDX17 is downregulated in EC tissues and correlates with poor prognosis.
  • DDX17 overexpression inhibits EC cell proliferation, migration, and invasion in vitro and in vivo.
  • METTL3-mediated m6A modification stabilizes DDX17 mRNA, involving IGF2BP2.
  • DDX17 exerts its tumor-suppressive effects via PI3K/AKT pathway inactivation.

Conclusions:

  • METTL3-mediated m6A modification stabilizes DDX17, suppressing EC progression.
  • The DDX17 tumor-suppressive function is mediated by IGF2BP2 and PI3K/AKT pathway inactivation.
  • DDX17 represents a promising therapeutic target for endometrial cancer.
Keywords:
DDX17Endometrial cancerIGF2BP2METTL3m6A modification

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