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Curcumin Modulates Hepatocellular Carcinoma by Reducing UNC119 Expression.

Zhenjiang Zhao1, Anshoo Malhotra2, Wu Yuan Seng3

  • 1Department of Radiology, Luoyang Orthopedic Hospital of Henan Province, Zhengzhou City, Henan Province, 450000, China.

Journal of Environmental Pathology, Toxicology and Oncology : Official Organ of the International Society for Environmental Toxicology and Cancer
|November 4, 2019
PubMed
Summary

Curcumin effectively targets UNC119, a protein overexpressed in liver cancer (HCC). This study shows curcumin inhibits HCC cell growth and spread by blocking key signaling pathways, improving tumor remission and survival in mice.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • UNC119 expression is elevated in hepatocellular carcinoma (HCC).
  • The precise role of UNC119 in HCC progression and the therapeutic potential of modulating its expression remain unclear.

Purpose of the Study:

  • To investigate the role of UNC119 in HCC development.
  • To explore curcumin's ability to modulate UNC119 expression and its downstream effects in HCC.
  • To elucidate the signaling pathways involved in UNC119-mediated HCC progression.

Main Methods:

  • Quantitative real-time PCR, Western blot, and immunohistochemical analyses were used to assess UNC119 expression in HCC cell lines and tissues.
  • In vitro and in vivo assays were performed to evaluate the impact of UNC119 on tumor cell proliferation, migration, invasion, and cell cycle progression.
  • The Wnt/β-catenin and TGF-β/EMT signaling pathways were investigated in relation to UNC119 function and curcumin's therapeutic effects.

Main Results:

  • UNC119 was significantly upregulated in HCC cells and tissues compared to normal controls.
  • Elevated UNC119 levels promoted HCC cell proliferation, migration, and invasion, driven by the Wnt/β-catenin and TGF-β/EMT pathways.
  • Curcumin treatment effectively inhibited HCC cell proliferation, growth, migration, and invasion by suppressing these signaling pathways.
  • Curcumin administration led to tumor remission and improved long-term survival in mice with HCC.

Conclusions:

  • UNC119 upregulation drives HCC progression through the Wnt/β-catenin and TGF-β/EMT pathways.
  • Curcumin demonstrates significant therapeutic potential against HCC by inhibiting UNC119-mediated signaling.
  • Targeting UNC119 with curcumin offers a promising strategy for HCC treatment.