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Delta-like 3 is silenced by HBx via histone acetylation in HBV-associated HCCs

Hiroki Hamamoto1, Kentaro Maemura2, Kentaro Matsuo3

  • 1Departments of General and Gastroenterological Surgery, Osaka Medical College, Takatsuki, 569-8686, Japan. sur154@osaka-med.ac.jp.

Scientific Reports
|March 21, 2018
PubMed

Insights

Hepatocellular carcinoma (HCC) progression involves suppressed Delta-like 3 (DLL3) expression, linked to Hepatitis B virus (HBV) infection. Epigenetic changes, including DNA methylation and histone modification, regulate DLL3 silencing in HCC.

Area of Science:

  • Hepatology
  • Oncology
  • Molecular Biology

Background:

  • Hepatocellular carcinoma (HCC) is a prevalent cancer with poor outcomes.
  • Delta-like 3 (DLL3) expression is silenced by DNA methylation in HCC, and its overexpression induces apoptosis.
  • The regulation of DLL3 during hepatocarcinogenesis remains unclear.

Purpose of the Study:

  • To investigate the regulatory mechanisms of DLL3 expression during hepatocarcinogenesis.
  • To determine the association between DLL3 silencing and viral infections, particularly Hepatitis B virus (HBV).

Main Methods:

  • Comparison of DLL3 expression in HepG2.2.15 (HBV-transformed) and HepG2 cells.
  • Assessment of DLL3 expression following Hepatitis B virus X protein (HBx) manipulation using small interfering RNA and overexpression.
  • Evaluation of DLL3 expression after treatment with a histone deacetylase inhibitor.

Main Results:

  • DLL3 expression is significantly lower in HBV-infected HepG2.2.15 cells compared to HepG2 cells.
  • HBx downregulates DLL3 expression, while HBx inhibition upregulates it.
  • Histone deacetylase inhibition increases DLL3 expression in HBV-infected cells.

Conclusions:

  • DLL3 silencing during hepatocarcinogenesis is associated with HBV infection.
  • Epigenetic mechanisms, including DNA methylation and histone modifications influenced by HBV, regulate DLL3 expression in HCC.

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