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Metformin inhibits glioma cells stemness and epithelial-mesenchymal transition via regulating YAP activity

Xuesong Yuan1, Wenfeng Wei1, Qing Bao1

  • 1Department of Neurosurgery, Changzhou Wujin People's Hospital, The Affliated Hospital of Jiangsu University, No.2 Yongning North Road, Changzhou, 213002, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|March 24, 2018
PubMed

Insights

Metformin suppresses glioma stemness and epithelial-mesenchymal transition by inhibiting YAP activity. This research reveals a novel mechanism for metformin

Area of Science:

  • Neuro-oncology
  • Cancer Biology
  • Molecular Mechanisms

Background:

  • Glioma stemness and epithelial-mesenchymal transition (EMT) drive tumor progression and treatment resistance.
  • Metformin is an antidiabetic drug with emerging anticancer properties.
  • Understanding metformin's role in glioma is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the effects of metformin on glioma stemness and EMT.
  • To elucidate the underlying molecular mechanisms of metformin's action in glioma cells.

Main Methods:

  • Glioma cell culture and spheroid formation assays.
  • Analysis of stemness markers (e.g., CD133) and EMT markers.
  • Western blotting to assess protein expression and localization (e.g., YAP).
  • Overexpression of YAP mutant to validate mechanistic pathways.

Main Results:

  • Metformin significantly suppressed glioma cell spheroid formation and size.
  • Metformin inhibited the expression of the stemness marker CD133.
  • Metformin attenuated transforming growth factor-beta (TGF-β)-induced EMT.
  • Metformin reduced nuclear YAP abundance, leading to cytoplasmic retention and decreased transcriptional activity.
  • Overexpression of a YAP mutant (YAP-5SA) partially reversed metformin's inhibitory effects.

Conclusions:

  • Metformin effectively inhibits glioma stemness and EMT.
  • The mechanism involves the regulation of YAP activity within the Hippo pathway.
  • Metformin represents a potential therapeutic agent for targeting glioma progression through YAP modulation.
Keywords:
CSCsGliomaHippoMetforminYAP/TAZ

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