CDK11(p58) protein kinase activity is associated with Bcl-2 down-regulation in pro-apoptosis pathway

Mol Cell Biochem. 2007 Oct;304(1-2):213-8. doi: 10.1007/s11010-007-9502-x. Epub 2007 May 22.


CDK11(p58), a G2/M-specific protein kinase, has been shown to be associated with apoptosis in many cell lines, with largely unknown mechanisms. Our previous study proved that CDK11(p58)-enhanced cycloheximide (CHX)-induced apoptosis in SMMC-7721 hepatocarcinoma cells. Here we report for the first time that ectopic expression of CDK11(p58) down-regulates Bcl-2 expression and its Ser70, Ser87 phosphorylation in CHX-induced apoptosis in SMMC-7721 cells. Overexpression of Bcl-2 counteracts the pro-apoptotic activity of CDK11(p58). Furthermore, we confirm that the kinase activity of CDK11(p58) is essential to the down-regulation of Bcl-2 as well as apoptosis. Taken together, these results demonstrate that CDK11(p58) down-regulates Bcl-2 in pro-apoptosis pathway depending on its kinase activity, which elicits survival signal in hepatocarcinoma cells.

MeSH terms

  • Apoptosis / genetics*
  • Carcinoma / genetics
  • Carcinoma / pathology
  • Cyclin-Dependent Kinases / genetics
  • Cyclin-Dependent Kinases / metabolism*
  • Cycloheximide / pharmacology
  • Down-Regulation*
  • Gene Expression Regulation, Neoplastic / drug effects
  • Genes, bcl-2*
  • Humans
  • Liver Neoplasms / genetics
  • Liver Neoplasms / pathology
  • Signal Transduction
  • Transfection
  • Tumor Cells, Cultured


  • Cycloheximide
  • CDK11a protein, human
  • Cyclin-Dependent Kinases