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Updated: Sep 11, 2025

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Activated MAFB in ovarian cancer promotes cytoskeletal remodeling and immune microenvironment suppression by

Qinke Li1,2, Siying Zhang1,2, Min Wang1

  • 1Department of Gynecology and Obstetrics, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Oncogene
|August 12, 2025
PubMed

Insights

MAFB promotes ovarian cancer progression by disrupting gene regulation and immune evasion. Targeting the MAFB-WTAP-CD55 pathway offers a new therapeutic strategy for ovarian cancer patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • The tumor microenvironment (TME) drives cancer progression via complex transcriptional networks.
  • Molecular mechanisms of immune evasion in ovarian cancer are not fully understood.

Purpose of the Study:

  • Identify key regulators of ovarian cancer progression and immune evasion.
  • Elucidate the molecular mechanisms underlying MAFB's role in ovarian cancer.

Main Methods:

  • Integration of immune dysfunction data from clinical cohorts.
  • Single-cell transcriptomics analysis.
  • Mechanistic studies on MAFB's interaction with the m6A methyltransferase complex.

Main Results:

  • MAFB identified as a key regulator, with elevated expression in advanced ovarian cancer stages.
  • MAFB antagonizes WTAP, leading to WNT5A and CD55 mRNA stabilization.
  • This axis promotes tumor invasiveness, M2 macrophage polarization, and regulatory T cell infiltration.

Conclusions:

  • MAFB promotes ovarian cancer progression through cytoskeletal remodeling and immune suppression.
  • The MAFB-WTAP-CD55 axis represents a novel regulatory mechanism linking transcription and epitranscriptomics.
  • This pathway is a potential therapeutic target for ovarian cancer.

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