CREB regulates AChE-R-induced proliferation of human glioblastoma cells

Chava Perry, Ella H. Sklan, Hermona Soreq*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


The cyclic adenosine monophosphate (AMP) response element-binding protein, CREB, often modulates stress responses. Here, we report that CREB suppresses the glioblastoma proliferative effect of the stress-induced acetylcholinesterase variant, AChE-R. In human U87MG glioblastoma cells, AChE-R formed a triple complex with protein kinase C (PKC) ε and the scaffold protein RACK1, enhanced PKCε phosphorylation, and facilitated BrdU incorporation. Either over-expressed CREB, or antisense destruction of AChE-R mRNA, PKC, or protein kinase A (PKA) inhibitors-but not CREB combined with PKC inhibition suppressed-this proliferation, suggesting that CREB's repression of this process involves a PKC-mediated pathway, whereas impaired CREB regulation allows AChE-R-induced, PKA-mediated proliferation of glioblastoma tumors.

Original languageEnglish
Pages (from-to)279-286
Number of pages8
Issue number3
StatePublished - 2004


  • Acetylcholinesterase
  • Antisense
  • CREB
  • Glioblastoma
  • PKCε


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