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Related Experiment Video

Updated: Dec 31, 2025

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis
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PRAS40 hyperexpression promotes hepatocarcinogenesis.

Zhaolai Qi1, Ting Zhang1, Lei Song2

  • 1Department of Pathophysiology, College of Basic Medical Sciences, Dalian Medical University, 9 South Lvshun Road, Dalian, Liaoning 116044, PR China.

Ebiomedicine
|January 6, 2020
PubMed
Summary

Loss of miR-124-3p leads to PRAS40 (proline-rich Akt substrate 40 kDa) overexpression and hyperphosphorylation, driving hepatocellular carcinoma (HCC) development. This discovery offers new avenues for HCC treatment strategies.

Keywords:
CarcinogenesisCell signalingHepatocellular carcinomaMicrornaMolecular oncology

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Hepatocellular carcinoma (HCC) is a prevalent cancer with poorly understood molecular drivers.
  • PRAS40 (AKT1S1) phosphorylation is elevated in several cancers, but its specific role in HCC remains unclear.

Purpose of the Study:

  • To investigate the role of PRAS40 and miR-124-3p in the development of hepatocellular carcinoma.
  • To elucidate the molecular mechanisms linking PRAS40, miR-124-3p, and HCC pathogenesis.

Main Methods:

  • Analysis of PRAS40 expression and phosphorylation in HCC patient samples and databases.
  • In vivo and in vitro functional studies of PRAS40 in HCC models.
  • Luciferase assays to confirm miR-124-3p targeting of PRAS40.
  • In Situ hybridization to assess miR-124-3p levels in HCC tissues.

Main Results:

  • PRAS40 levels (mRNA, protein, phosphorylation) are significantly increased in HCC and correlate with poor prognosis.
  • PRAS40 deficiency suppresses hepatocarcinogenesis and impairs Akt activation in mice.
  • miR-124-3p directly targets PRAS40, and its levels are inversely correlated with PRAS40 in HCC.
  • Restoration of miR-124-3p inhibits HCC cell proliferation, an effect partially reversed by PRAS40.

Conclusions:

  • PRAS40 hyperexpression, driven by miR-124-3p loss, promotes hepatocellular carcinoma.
  • Targeting the PRAS40/miR-124-3p axis presents a potential therapeutic strategy for HCC.