Study on the Inhibitory Effect of Curcumin on GBM and Its Potential Mechanism

Xiaotao Su1, Shaohua Chen2, Hongyu Lu1

  • 1Department of Neurology, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, People's Republic of China.

Abstract

Insights

Curcumin shows potential against glioblastoma (GBM) by targeting ENO1, a gene involved in glycolysis. This natural compound inhibits GBM cell migration and invasion, offering a new therapeutic avenue for this aggressive brain cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Natural Products Chemistry

Background:

  • Glioblastoma (GBM) is a prevalent and aggressive central nervous system (CNS) malignancy with limited treatment options.
  • Curcumin, a natural compound, exhibits anticancer properties, but its specific targets and mechanisms in GBM remain largely unelucidated.

Purpose of the Study:

  • To identify potential therapeutic targets of curcumin in glioblastoma.
  • To investigate the effects of curcumin on GBM cell behavior and apoptosis.
  • To explore the role of identified target genes in GBM prognosis and cellular pathways.

Main Methods:

  • Bioinformatic analysis of GBM datasets to identify curcumin target genes.
  • Survival analysis using GEPIA database for prognostic significance.
  • In vitro assays (CCK-8, scratch, Transwell) to assess curcumin's effect on GBM cell migration, invasion, and apoptosis.
  • RT-qPCR and Western blotting for gene expression analysis.

Main Results:

  • Sixteen potential target genes of curcumin in GBM were identified, with ENO1, MMP2, and PRKD2 significantly impacting prognosis.
  • ENO1 was found to be enriched in the glycolytic pathway.
  • Curcumin treatment inhibited U251 GBM cell migration and invasion while promoting apoptosis.

Conclusions:

  • Enolase 1 (ENO1) is identified as a potential molecular target for curcumin's anti-GBM activity.
  • Curcumin demonstrates therapeutic potential against glioblastoma by modulating ENO1 and affecting key cellular processes like migration, invasion, and apoptosis.

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