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KMID : 0620920020340010027
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Experimental & Molecular Medicine
2002 Volume.34 No. 1 p.27 ~ p.31
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Differential modulation of zinc-stimulated p21Cip/WAF1 and cyclin D1 induction by inhibition of P13 kinase in HT-29 colorectal cancer cells
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Kang Yell Choi/So Young Oh
Ki Sook Park/Jin Ah Kim/Kang Yell Choi
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Abstract
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Activation of the extra cellular signal regulated kinase (ERK) pathway is involved in both proliferation and growth arrest of cells depending on intensity and duration of stimuli. In this study, we have elucidated differential regulation of the zinc-stimulated p21(CiP/WAF1) and cyclin D1 activation by inhibition of phosphoinositide 3-kinase (PI3K). In HT-29 colorectal cancer cells, the ERK activities were increased by zinc, which was accompanied by the induction of p21(Cip/WAF1) and cyclin D1. However, in the HT-29 cells pre-treated with PI3K inhibitor, LY294002, zinc induced further the p21(CiP/WAF) induction whereas abrogated cyclin D1 induction. In addition, the induction of p21(Cip/WAF1) expression completely inhibited the incorporation of bromodeoxyuridine (BrdU) into the nucleus, indicating that p21(CiP/WAF1) is an important indicator for ERK-dependent growth arrest. These studies suggest presence of an inter-related regulatory mechanism of cell proliferation by ERK and PI3K pathways.
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KEYWORD
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MAP kinase, ERK, Zinc, cyclin D1, p21Cip/WAF1, cell growth regulation, P13 kinase,
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