Curcumin-Mediated Induction of Apoptosis in Human Glioma CHME Cells

Med Sci Monit Basic Res. 2018 Dec 10;24:216-224. doi: 10.12659/MSMBR.912313.


BACKGROUND Curcumin has clear anti-tumor activity in various carcinomas. It regulates various signaling pathways like Wnt/β-catenin and JAK2/STAT3, which play vital roles in cell proliferation of several carcinomas, but to the best of our knowledge, there are currently no published reports on human glioma CHME cells. Therefore, the aim of this study was to explore the effect of curcumin on human glioma CHME cells. MATERIAL AND METHODS The CHME cell line was purchased from American Type Culture Collection (ATCC). The expressions of caspases 3, caspases 9, PARP, BAX, and BCL2 were detected by Western blot. Annexin V FITC, mitochondrial membrane potential, and reactive oxygen species were detected by flow cytometry. DAPI staining was detected by fluorescence microscopy. Cell viability was assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay. RESULTS We found that curcumin has cytotoxic activity in human glioma CHME cells, as shown by DAPI staining, annexin V/PI, and nuclear morphology. We found that cell growth decreased with increased concentration of curcumin, as well as sowing effects on expression of caspase-3, caspase-9, and cleavage of PARP, which suggests apoptotic cascade activity. The increase in reactive oxygen species and loss of mitochondrial membrane potential (Δψmt) in concentration-dependent manners suggests biochemical induction of apoptosis in CHME cells. CONCLUSIONS Curcumin has effective anticancer activity in human glioma CHME cells by inducing the apoptotic pathway.

MeSH terms

  • Apoptosis / drug effects*
  • Caspase 3 / metabolism
  • Caspase 9 / metabolism
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Curcumin / pharmacology*
  • Glioma / drug therapy*
  • Glioma / metabolism
  • Glioma / pathology
  • Humans
  • Mitochondria / drug effects
  • Reactive Oxygen Species / metabolism
  • Signal Transduction / drug effects


  • Reactive Oxygen Species
  • CASP3 protein, human
  • CASP9 protein, human
  • Caspase 3
  • Caspase 9
  • Curcumin