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Molecular mechanism of hepatitis B virus (HBV) on suppression of raf kinase inhibitor protein (RKIP) expression

Xiao-Ke Cheng1, Guo-Zheng Yu2, Xiao-Dong Li1,3

  • 1Center for Evidence-Based Medicine, Huaihe Hospital of Henan University, Kaifeng 475000, Henan Province, China.

Oncotarget
|December 1, 2016
PubMed

Insights

Hepatitis B virus (HBV) X protein suppresses Raf kinase inhibitor protein (RKIP) expression in liver cancer by inhibiting transcription and enhancing promoter methylation. RKIP may serve as a marker but lacks tumor-suppressing effects in this context.

Area of Science:

  • Molecular biology
  • Hepatology
  • Oncology

Background:

  • Raf kinase inhibitor protein (RKIP) is a mitogen-activated protein kinase pathway suppressor implicated in human cancers.
  • The mechanism by which hepatitis B virus (HBV) influences RKIP expression remains unclear.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying HBV-mediated regulation of RKIP expression in liver cancer.
  • To determine if RKIP functions as a tumor suppressor in HBV-infected liver tissues.

Main Methods:

  • Comparative analysis of RKIP expression in 107 paired liver cancer and adjacent non-cancerous tissues.
  • Identification of HBV-encoded proteins affecting RKIP expression using cell-based assays.
  • Investigation of transcriptional regulation and promoter methylation of RKIP in Huh7 cells.

Main Results:

  • HBV X (HBX) protein significantly downregulates RKIP expression.
  • HBX interacts with AP1 to inhibit RKIP transcription.
  • HBV infection enhances RKIP promoter methylation, and RKIP exhibits no tumor-suppressing effect in HBV-infected liver cancer.

Conclusions:

  • HBV suppresses RKIP expression primarily through the HBX protein via transcriptional inhibition and promoter methylation.
  • RKIP can serve as a potential molecular marker for HBV-infected liver cancer.
  • RKIP does not possess a tumor-suppressing role in the context of HBV-associated liver cancer.
Keywords:
AP1proteinHBVRKIPliver cancerpromoter methylation

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