Amentoflavone Induces Apoptosis and Inhibits NF-ĸB-modulated Anti-apoptotic Signaling in Glioblastoma Cells

In Vivo. Mar-Apr 2018;32(2):279-285. doi: 10.21873/invivo.11235.


The goal of the present study was to investigate anticancer effect of amentoflavone on glioblastoma cells in vitro. Our results demonstrated that amentoflavone not only significantly reduced cell viability, nuclear factor-ĸappa B (NF-ĸB) activation, and protein expression of cellular Fas-associated protein with death domain-like interleukin 1 beta-converting enzyme inhibitory protein (C-FLIP) and myeloid cell leukemia 1 (MCL1), but significantly triggered cell accumulation at the sub-G1 phase, loss of mitochondrial membrane potential, and expression of active caspase-3 and -8. In order to verify the effect of NF-ĸB inhibitor on expression of anti-apoptotic proteins, we performed western blotting. We found that the of NF-ĸB inhibitor or amentoflavone markedly diminished protein levels of MCL1 and C-FLIP. Taken all together, our findings show that amentoflavone induces intrinsic and extrinsic apoptosis and inhibits NF-ĸB-modulated anti-apoptotic signaling in U-87 MG cells in vitro.

Keywords: Glioblastoma; NF-ĸB; amentoflavone; apoptosis.

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis / genetics
  • Apoptosis Regulatory Proteins / genetics
  • Apoptosis Regulatory Proteins / metabolism
  • Biflavonoids / pharmacology*
  • Caspase 3 / metabolism
  • Caspase 8 / metabolism
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Cytochrome P-450 Enzyme Inhibitors / pharmacology*
  • Glioblastoma / genetics
  • Glioblastoma / metabolism*
  • Humans
  • Membrane Potential, Mitochondrial / drug effects
  • NF-kappa B / metabolism*
  • Signal Transduction / drug effects*


  • Apoptosis Regulatory Proteins
  • Biflavonoids
  • Cytochrome P-450 Enzyme Inhibitors
  • NF-kappa B
  • amentoflavone
  • Caspase 3
  • Caspase 8