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SOS1 regulates HCC cell epithelial-mesenchymal transition via the PI3K/AKT/mTOR pathway

Yonghe Li1, Yaolin Yin1, Yi He1

  • 1Department of Hepatobiliary Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong, China; Institute of Hepato-Biliary-Pancreatic-Intestinal Disease, North Sichuan Medical College, Nanchong, China.

Biochemical and Biophysical Research Communications
|November 20, 2022
PubMed

Insights

Son of sevenless homolog 1 (SOS1) promotes hepatocellular carcinoma (HCC) invasion and metastasis by activating the PI3K/AKT/mTOR pathway and epithelial-mesenchymal transition (EMT). Targeting SOS1 may offer a new therapeutic strategy for liver cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Hepatocellular carcinoma (HCC) is a major global health concern with limited effective treatments.
  • Understanding the molecular mechanisms driving HCC invasion and metastasis is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of son of sevenless homolog 1 (SOS1) in the invasion and metastasis of hepatocellular carcinoma (HCC) cells.
  • To explore the underlying molecular pathways, including epithelial-mesenchymal transition (EMT) and the PI3K/AKT/mTOR pathway, influenced by SOS1.

Main Methods:

  • SOS1 knockdown and overexpression were achieved in HCC cell lines (HepG2, Huh7) using siRNA and lentivirus.
  • Quantitative PCR (q-PCR) and Western blotting (WB) were used to analyze gene and protein expression levels.
  • Transwell assays assessed cell invasion and migration in vitro, and a lung metastasis model evaluated in vivo metastatic potential.

Main Results:

  • High SOS1 expression correlated with worse prognosis in human HCC.
  • SOS1 knockout significantly reduced HCC cell invasion, migration, and lung metastasis in mice.
  • SOS1 inhibition suppressed EMT and the PI3K/AKT/mTOR pathway in HCC cells, while SOS1 overexpression had opposite effects.

Conclusions:

  • SOS1 promotes HCC invasion, migration, and metastasis, potentially by inducing EMT via activation of the PI3K/AKT/mTOR pathway.
  • SOS1 represents a promising therapeutic target for hepatocellular carcinoma.
Keywords:
Epithelial-mesenchymal-transitionHepatocellular carcinomaPI3K/AKT/mTORSOS1

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