CDK5 is a novel regulatory protein in PPARγ ligand-induced antiproliferation

Eugene Kim, Fei Chen, Chia Chi Wang, Lawrence Harrison

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Cyclin-dependent kinase 5 (Cdk5) is a member of the cyclin-dependent kinase family and has been studied mainly in the differentiation of post-mitotic neurons. The purpose of this study was to determine the presence of cdk5 expression and activity in colon cancer cells and to investigate its role in the regulation of PPARγ ligand-induced antiproliferation. We observed that cdk5 protein levels and kinase activity were elevated in both HT-29 cells and human tumor tissue in comparison to decreased levels in normal colonic mucosa. To elucidate cdk5's role in PPARγ ligand-induced antiproliferation of colon cancer cells, HT-29 cells were treated with ciglitazone. A dose- and time-dependent decrease in cell proliferation were observed after ciglitazone exposure, which correlated with a decrease in cdk5 protein expression and kinase activity. Importantly, these ciglitazone-induced antiproliferative changes were reversed when cdk5 was overexpressed. Although present, p35, the regulatory protein of cdk5, showed no significant changes in protein expression with the introduction of ciglitazone. This is the first report of cdk5/p35 expression and kinase activity in colon cancer cells, which is associated with ciglitazone-induced antiproliferation in HT-29 cells.

Original languageEnglish (US)
Pages (from-to)191-194
Number of pages4
JournalInternational Journal of Oncology
Volume28
Issue number1
StatePublished - Jan 1 2006
Externally publishedYes

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Peroxisome Proliferator-Activated Receptors
Cyclin-Dependent Kinase 5
HT29 Cells
Ligands
Colonic Neoplasms
Proteins
Cyclin-Dependent Kinases
Mucous Membrane
Phosphotransferases
Cell Proliferation
ciglitazone
Neurons
Neoplasms

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

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title = "CDK5 is a novel regulatory protein in PPARγ ligand-induced antiproliferation",
abstract = "Cyclin-dependent kinase 5 (Cdk5) is a member of the cyclin-dependent kinase family and has been studied mainly in the differentiation of post-mitotic neurons. The purpose of this study was to determine the presence of cdk5 expression and activity in colon cancer cells and to investigate its role in the regulation of PPARγ ligand-induced antiproliferation. We observed that cdk5 protein levels and kinase activity were elevated in both HT-29 cells and human tumor tissue in comparison to decreased levels in normal colonic mucosa. To elucidate cdk5's role in PPARγ ligand-induced antiproliferation of colon cancer cells, HT-29 cells were treated with ciglitazone. A dose- and time-dependent decrease in cell proliferation were observed after ciglitazone exposure, which correlated with a decrease in cdk5 protein expression and kinase activity. Importantly, these ciglitazone-induced antiproliferative changes were reversed when cdk5 was overexpressed. Although present, p35, the regulatory protein of cdk5, showed no significant changes in protein expression with the introduction of ciglitazone. This is the first report of cdk5/p35 expression and kinase activity in colon cancer cells, which is associated with ciglitazone-induced antiproliferation in HT-29 cells.",
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CDK5 is a novel regulatory protein in PPARγ ligand-induced antiproliferation. / Kim, Eugene; Chen, Fei; Wang, Chia Chi; Harrison, Lawrence.

In: International Journal of Oncology, Vol. 28, No. 1, 01.01.2006, p. 191-194.

Research output: Contribution to journalArticle

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