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The aPKCι blocking agent ATM negatively regulates EMT and invasion of hepatocellular carcinoma

C Q Ma1, Y Yang1, J M Wang1

  • 1Department of Biliary and Pancreatic Surgery/Cancer Research Center Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Cell Death & Disease
|March 22, 2014
PubMed

Insights

Atypical protein kinase C ι (aPKCι) drives hepatocellular carcinoma (HCC) cell invasion. The agent aurothiomalate (ATM) blocks aPKCι, inhibiting EMT and HCC cell proliferation, suggesting ATM as a potential targeted therapy.

Area of Science:

  • Hepatocellular carcinoma (HCC) research
  • Cancer cell biology
  • Molecular signaling pathways

Background:

  • Epithelial-to-mesenchymal transition (EMT) is crucial for hepatocellular carcinoma (HCC) invasion and metastasis.
  • Understanding atypical protein kinase C ι (aPKCι) signaling is key to targeting HCC development.

Purpose of the Study:

  • To investigate the role of aPKCι signaling in HCC EMT.
  • To identify a potential therapeutic agent for HCC targeting aPKCι.

Main Methods:

  • Established an HCC EMT cell model (MMH-RT cells) using immortalized murine hepatocytes.
  • Utilized transforming growth factor-β1 (TGF-β1) to induce EMT and aPKCι overexpression.
  • Administered aurothiomalate (ATM), an aPKCι blocking agent, to assess its effects on HCC cells.

Main Results:

  • Transforming growth factor-β1 (TGF-β1) induced EMT and aPKCι overexpression in MMH-RT cells.
  • Aurothiomalate (ATM) inhibited EMT and reduced hepatocyte invasion.
  • ATM selectively inhibited proliferation of mesenchymal and HepG2 cells while inducing apoptosis, with minimal effects on epithelial cells.

Conclusions:

  • aPKCι serves as a significant biomarker for tumor EMT, invasion, and malignancy in HCC.
  • Aurothiomalate (ATM) demonstrates potential as a targeted therapeutic agent for HCC treatment.

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