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(Z)-3,5,4'-Trimethoxystilbene Limits Hepatitis C and Cancer Pathophysiology by Blocking Microtubule Dynamics and

Charles B Nguyen1, Hari Kotturi2, Gulam Waris3

  • 1College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.

Cancer Research
|June 12, 2016
PubMed

Insights

(Z)-3,5,4'-trimethoxystilbene (Z-TMS) shows promise in treating liver cancer by targeting both hepatitis C virus (HCV) and cancer stem cell (CSC) properties. This compound offers a dual approach for advanced liver disease, reducing tumor markers and protecting liver cells.

Area of Science:

  • Hepatocellular carcinoma (HCC) research
  • Drug discovery and development
  • Cancer stem cell biology

Background:

  • Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality globally.
  • Chronic hepatitis C virus (HCV) infection is a major risk factor for HCC development, associated with increased cancer stem cell (CSC) markers.
  • There is a critical need for treatments that target both viral replication and CSC properties in advanced liver disease.

Purpose of the Study:

  • To evaluate the therapeutic potential of (Z)-3,5,4'-trimethoxystilbene (Z-TMS) against HCC and HCV.
  • To investigate Z-TMS's effects on CSC markers, specifically DCLK1, in a mouse model of liver injury.
  • To elucidate the mechanisms by which Z-TMS exerts its anti-cancer effects in hepatoma and drug-resistant lung cancer cells.

Main Methods:

  • In vitro and in vivo studies using hepatoma cells and a diethylnitrosamine/carbon tetrachloride-induced mouse liver injury model.
  • Assessment of Z-TMS's cytotoxicity, anti-HCV activity, and effects on DCLK1 expression.
  • Analysis of cell-cycle progression, protein expression (CDK1, p21, Akt), autophagy, and nuclear fragmentation in cancer cells.

Main Results:

  • Z-TMS demonstrated potent anti-HCV and antitumor activities without significant hepatotoxicity.
  • In mice, Z-TMS protected against liver injury by reducing DCLK1 expression and improving histological outcomes.
  • Z-TMS induced DCLK1 bundling with microtubules, G2-M cell-cycle arrest, and inhibited Akt phosphorylation in hepatoma cells.
  • Z-TMS inhibited proliferation of erlotinib-resistant lung cancer cells, likely through autophagy promotion and nuclear fragmentation.

Conclusions:

  • Z-TMS is a unique therapeutic agent with the potential to treat HCV and eliminate neoplastic cells in chronic liver diseases like HCC.
  • Z-TMS may also be effective against drug-resistant cancers, including lung, pancreas, colon, and intestinal cancers, where DCLK1 is implicated in tumorigenesis.

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