Apoptotic Effects of Cordycepin Through the Extrinsic Pathway and p38 MAPK Activation in Human Glioblastoma U87MG Cells

J Microbiol Biotechnol. 2016 Feb;26(2):309-14. doi: 10.4014/jmb.1507.07090.


We first demonstrated that cordycepin inhibited cell growth and triggered apoptosis in U87MG cells with wild-type p53, but not in T98G cells with mutant-type p53. Western blot data revealed that the levels of procaspase-8, -3, and Bcl-2 were downregulated in cordycepintreated U87MG cells, whereas the levels of Fas, FasL, Bak, cleaved caspase-3, -8, and cleaved PARP were upregulated, indicating that cordycepin induces apoptosis by activating the death receptor-mediated pathway in U87MG cells. Cordycepin-induced apoptosis could be suppressed by only SB203580, a p38 MAPK-specific inhibitor. These results suggest that cordycepin triggered apoptosis in U87MG cells through p38 MAPK activation and inhibition of the Akt survival pathway.

Keywords: Cordycepin; U87MG cell; apoptosis; extrinsic pathway; p38 MAPK.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antifungal Agents / pharmacology
  • Apoptosis / drug effects*
  • Caspase 3 / metabolism
  • Caspase 8 / metabolism
  • Cell Cycle / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects*
  • Deoxyadenosines / pharmacology*
  • Fas Ligand Protein / metabolism
  • Glioblastoma*
  • Humans
  • Signal Transduction
  • bcl-2-Associated X Protein / genetics
  • bcl-2-Associated X Protein / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism


  • Antifungal Agents
  • Deoxyadenosines
  • FASLG protein, human
  • Fas Ligand Protein
  • bcl-2-Associated X Protein
  • p38 Mitogen-Activated Protein Kinases
  • Caspase 3
  • Caspase 8
  • cordycepin