Anisomycin affects both pro- and antiapoptotic mechanisms in PC12 cells

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32 Citations (Scopus)


Survival and differentiation of PC12 cells depend on the proper balance between the activities of several mitogen-activated protein kinase (MAPK) pathways. We have previously shown that low, nontoxic doses of anisomycin stimulated these MAPKs as well as the expression of several early-response genes and inhibited NGF-induced neurite formation. In the present work we show that protein synthesis-inhibiting concentrations of anisomycin, in contrast, cause apoptosis of PC12 cells. To try to characterize the apoptosis-inducing mechanisms of anisomycin we compared the signaling effects of subinhibitory and inhibitory drug concentrations. Anisomycin in a nontoxic dosis activates the same MAPK pathways and early-response genes as in protein synthesis inhibiting concentrations. In contrast, while the subinhibitory anisomycin treatment stimulates Akt and induces Bcl-2, two antiapoptotic proteins, the translation-inhibiting concentration of the drug prevents these survival-promoting biochemical events. Anisomycin thus triggers both pro- and antiapoptotic processes in PC12 cells; stimulation of stress-responsive MAPK cascades is not sufficient to mediate apoptotic signaling: The inhibition of key antiapoptotic proteins appears to be more important for PC12 cell death by anisomycin treatment. (C) 2000 Academic Press.

Original languageEnglish
Pages (from-to)550-556
Number of pages7
JournalBiochemical and biophysical research communications
Issue number3
Publication statusPublished - Nov 30 2000


  • Akt
  • Anisomycin
  • Apoptosis
  • Bcl-2
  • Gene expression
  • Mitogen-activated protein kinases
  • Nerve growth factor
  • Neuronal differentiation
  • PC12 cells

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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