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BATF Drives Cervical Cancer Progression and Immune Evasion by Regulating the STAT1-PD-L1 Axis

Jun Zhang1, Yang Zhang1, Jinwei Zhang1

  • 1Department of Gynecology, The Affliated Wuxi People's Hospital of Nanjing Medical University, Wuxi Medical Center, Nanjing Medical University, Wuxi People's Hospital, Wuxi, Jiangsu 214023, China.

Iranian Journal of Immunology : IJI
|March 6, 2026
PubMed
Abstract

Insights

The transcription factor BATF promotes cervical cancer growth and immune evasion by activating STAT1 and PD-L1. Targeting BATF may improve cancer immunotherapy outcomes.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Cervical cancer progression involves immune evasion, notably through PD-L1 suppressing T cell activity.
  • The transcription factor BATF's role in tumor immunity is recognized but not fully understood in cancer.

Purpose of the Study:

  • To investigate the BATF-STAT1-PD-L1 signaling axis in cervical cancer progression.
  • To elucidate the role of BATF in regulating tumor immunity and progression.

Main Methods:

  • Analysis of BATF expression in cervical cancer tissues and cell lines.
  • Functional assays (proliferation, apoptosis, autophagy, migration) following BATF knockdown.
  • Chromatin immunoprecipitation and Western blot to assess STAT1 regulation.
  • Flow cytometry for PD-L1 expression and in vivo xenograft models for tumor growth and immunotherapy response.

Main Results:

  • BATF was upregulated in cervical cancer, promoting tumor growth, metastasis, and immune evasion.
  • BATF knockdown inhibited proliferation, enhanced apoptosis and autophagy, and reduced migration.
  • BATF transcriptionally activated STAT1, leading to PD-L1 induction. BATF suppression increased CD8+ T cell infiltration and enhanced PD-L1 blockade efficacy.

Conclusions:

  • BATF drives cervical cancer progression via STAT1 and PD-L1 modulation.
  • Targeting BATF presents a potential strategy to enhance anti-tumor immunity and immunotherapy efficacy.
Keywords:
BATFCervical cancerCheckpoint blockadeImmune evasionPD-L1 STAT1

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