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PCK1 attenuates tumor stemness via activating the Hippo signaling pathway in hepatocellular carcinoma.

Rui Liu1, Yi Liu1, Wenlu Zhang1

  • 1Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China.

Genes & Diseases
|April 1, 2024
PubMed
Summary
This summary is machine-generated.

Phosphoenolpyruvate carboxylase 1 (PCK1) inhibits liver cancer stem cell self-renewal and tumorigenesis. PCK1 enhances sorafenib sensitivity and may offer a combined treatment strategy with verteporfin for hepatocellular carcinoma.

Keywords:
Cancer stem cellsChemoresistanceGluconeogenesisHepatocellular carcinomaYAP

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Area of Science:

  • Biochemistry
  • Oncology
  • Cell Biology

Background:

  • Liver cancer stem cells utilize glycolysis for energy.
  • Phosphoenolpyruvate carboxylase 1 (PCK1) is downregulated in hepatocellular carcinoma (HCC), correlating with poor prognosis.
  • The role of PCK1 deficiency in promoting hepatoma cell stemness and HCC oncogenesis requires clarification.

Purpose of the Study:

  • To investigate the effect of PCK1 on hepatoma cell stemness and HCC progression.
  • To determine if PCK1 influences sensitivity to sorafenib.
  • To elucidate the mechanism by which PCK1 affects cancer stem cells, including its interaction with the Hippo pathway.

Main Methods:

  • Assessed PCK1's impact on hepatoma cell self-renewal and cancer stem cell marker expression.
  • Evaluated PCK1's effect on HCC cell sensitivity to sorafenib.
  • Investigated PCK1's role in activating the Hippo pathway via YAP phosphorylation and translocation.
  • Utilized verteporfin to modulate stemness and apoptosis in combination with sorafenib.

Main Results:

  • PCK1 significantly inhibited hepatoma cell self-renewal and reduced cancer stem cell marker mRNA levels.
  • PCK1 suppressed tumor formation (tumorigenesis) and increased sensitivity to sorafenib in HCC cells.
  • PCK1 activated the Hippo pathway by promoting YAP phosphorylation, thereby inhibiting its nuclear translocation.
  • Verteporfin decreased hepatoma cell stemness and enhanced sorafenib's pro-apoptotic effects.

Conclusions:

  • PCK1 deficiency promotes hepatoma cell stemness and HCC oncogenesis.
  • PCK1 enhances HCC cell sensitivity to sorafenib through Hippo pathway activation.
  • Combined treatment with verteporfin and sorafenib presents a potential therapeutic strategy for hepatocellular carcinoma.