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Oncofetal gene SALL4 reactivation by hepatitis B virus counteracts miR-200c in PD-L1-induced T cell exhaustion

Cheng Sun1,2, Peixiang Lan3, Qiuju Han3

  • 1The CAS Key Laboratory of Innate Immunity and Chronic Disease and Institute of Immunology, School of Life Science and Medical Center, University of Science and Technology of China, Hefei, 230027, Anhui, China.

Nature Communications
|March 30, 2018
PubMed

Insights

Hepatitis B virus (HBV) infection reactivates SALL4, which suppresses miR-200c, leading to PD-L1 upregulation and T cell exhaustion in liver cancer. Restoring miR-200c may reverse this immune suppression.

Area of Science:

  • Immunology
  • Oncology
  • Virology

Background:

  • Chronic viral infections and tumors induce T cell exhaustion via coinhibitory ligands.
  • Host factors controlling coinhibitory ligand expression and viral disruption of this control remain unclear.

Purpose of the Study:

  • Investigate the relationship between SALL4, PD-L1, and miR-200c in HBV-related hepatocellular carcinoma.
  • Elucidate the mechanism by which HBV influences coinhibitory ligand expression and T cell exhaustion.

Main Methods:

  • Correlation analysis of SALL4, PD-L1, and miR-200c in 98 HBV-related hepatocellular carcinoma patient tumors.
  • In vitro studies on miR-200c targeting of CD274 (PD-L1) 3'-UTR.
  • Analysis of HBV-induced STAT3 activation and SALL4 re-expression.

Main Results:

  • A negative correlation was observed between SALL4/PD-L1 and miR-200c in patient tumors.
  • Lower SALL4/PD-L1 and higher miR-200c correlated with improved patient survival.
  • miR-200c overexpression reversed HBV-mediated PD-L1 upregulation and CD8+ T cell exhaustion.
  • HBV-induced STAT3 activation re-expressed SALL4, inhibiting miR-200c transcription.

Conclusions:

  • An HBV-pSTAT3-SALL4-miR-200c axis regulates PD-L1 expression in hepatocellular carcinoma.
  • Targeting this axis offers a potential therapeutic strategy to reverse virus-induced immune exhaustion.

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