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RSL3 induced autophagic death in glioma cells via causing glycolysis dysfunction

Xuanzhong Wang1, Shan Lu1, Chuan He1

  • 1Department of Neurosurgery, First Hospital of Jilin University, Changchun, 130021, China; Research Center of Neuroscience, First Hospital of Jilin University, Changchun, 130021, China.

Biochemical and Biophysical Research Communications
|August 26, 2019
PubMed

Insights

RSL3 compound induces glioma cell death by disrupting glycolysis and activating autophagy. Supplementing with sodium pyruvate counteracts these effects, highlighting a novel therapeutic pathway for glioma treatment.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • RSL3 inactivates glutathione peroxidase 4 (GPX4), inducing ferroptosis.
  • The precise role of RSL3 in glioma cell death is not fully understood.

Purpose of the Study:

  • To investigate the mechanism of RSL3-induced glioma cell death.
  • To explore the relationship between RSL3, glycolysis, and autophagy in glioma cells.

Main Methods:

  • In vitro cell viability assays and Western blotting.
  • In vivo tumor growth inhibition studies.
  • Analysis of cellular ATP, pyruvate, and key glycolytic enzyme levels.

Main Results:

  • RSL3 inhibited glioma cell viability and induced cell death in a dose-dependent manner.
  • RSL3-induced cell death involved autophagy and was linked to impaired glycolysis.
  • Supplementation with sodium pyruvate reversed RSL3-induced autophagy and cell death.

Conclusions:

  • RSL3 induces autophagic cell death in glioma cells by causing glycolysis dysfunction.
  • Targeting glycolysis may represent a therapeutic strategy for glioma.
Keywords:
AutophagyGliomaGlycolysis dysfunctionRSL3

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