Involvement of both extracellular signal-regulated kinase and c-jun N-terminal kinase pathways in the 12-O- tetradecanoylphorbol-13-acetate-induced upregulation of p21Cip1 in colon cancer cells

研究成果: 雜誌貢獻文章同行評審

36 引文 斯高帕斯(Scopus)

摘要

Protein kinase C (PKC), a family of serine-threonine kinases, has been implicated in the regulation of colon tumorigenesis. However, the specific isoform of PKC involved in this process is not clear. In the present study, we found that treatment of the cultured human colon cancer cell line COLO-205 with a PKC agonist, 12-O-tetradecanoylphorbol-13-acetate (TPA), resulted in cell-cycle arrest at the G0/G1 phase, decrease in cell number, PKCγ isoform translocation, and upregulation of p21Cip1 protein. Pretreatment of the cells with a PKC inhibitor, staurosporine, prevented the TPA-induced upregulation of p21Cip1 protein. Based on the findings of the present study including that (a) both extracellular signal-regulated kinase (ERK) and c-jun N-terminal kinase (JNK) were activated in the TPA-treated COLO-205 cells, (b) pretreatment with the mitogen-activated protein kinase kinase inhibitor PD98059 but not with the p38 mitogen-activated protein kinase inhibitor SB203580 blocked the TPA-induced p21Cip1 in COLO-205 cells, and (c) transient transfection of the COLO-205 cells with dominant negative ERK or JNK plasmid significantly suppressed the TPA-induced p21Cip1 protein induction, we conclude that both the ERK and JNK pathways are involved in the TPA-induced upregulation of p21Cip1 protein in the COLO-205 cells.
原文英語
頁(從 - 到)21-28
頁數8
期刊Molecular Carcinogenesis
35
發行號1
DOIs
出版狀態已發佈 - 九月 2002

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Biology

指紋 深入研究「Involvement of both extracellular signal-regulated kinase and c-jun N-terminal kinase pathways in the 12-O- tetradecanoylphorbol-13-acetate-induced upregulation of p21<sup>Cip1</sup> in colon cancer cells」主題。共同形成了獨特的指紋。

引用此