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Exploring the Potential of Mesenchymal Stem Cell Sheet on The Development of Hepatocellular Carcinoma In Vivo
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Metformin reverses stem cell‑like HepG2 sphere formation and resistance to sorafenib by attenuating

Yan Feng1, Xing Guo1, Xinping Huang1

  • 1Research Department, Affiliated Cancer Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.

Molecular Medicine Reports
|August 15, 2018
PubMed

Insights

Metformin can overcome drug resistance in liver cancer by targeting cancer stem cells (CSCs). This study shows metformin reduces CSCs and enhances sorafenib sensitivity, likely by reversing epithelial-mesenchymal transformation (EMT).

Area of Science:

  • Hepatocellular carcinoma research
  • Cancer stem cell biology
  • Pharmacology

Background:

  • Cancer stem cells (CSCs) are implicated in liver cancer recurrence and drug resistance.
  • HepG2 cell spheres, enriched for stem-like properties, display resistance to sorafenib.

Purpose of the Study:

  • To investigate the effect of metformin on CSC-like HepG2 spheres.
  • To determine if metformin can re-sensitize these cells to sorafenib.

Main Methods:

  • Enrichment of stem cell-like HepG2 spheres using conditioned medium.
  • Treatment of spheres with metformin and sorafenib.
  • Assessment of sphere formation, size, and drug sensitivity.
  • Western blotting to analyze epithelial-mesenchymal transformation (EMT) markers.

Main Results:

  • Stem-like HepG2 spheres showed increased resistance to sorafenib.
  • Metformin reduced the number and size of these spheres.
  • Metformin increased the sensitivity of HepG2 spheres to sorafenib.
  • Low-dose metformin reversed the EMT process in HepG2 spheres.

Conclusions:

  • Metformin enhances sorafenib sensitivity in liver cancer.
  • This effect is likely mediated by the reversal of EMT and reduction of CSCs.
  • Metformin shows potential as an adjuvant therapy for liver cancer.

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