Differential modulation of zinc-stimulated p21Cip/WAF1 and cyclin D1 induction by inhibition of PI3 kinase in HT-29 colorectal cancer cells

So Young Oh; Ki Sook Park; Jin Ah Kim; Kang Yell Choi

doi:10.1038/emm.2002.4

Differential modulation of zinc-stimulated p21^Cip/WAF1 and cyclin D1 induction by inhibition of PI3 kinase in HT-29 colorectal cancer cells

So Young Oh, Ki Sook Park, Jin Ah Kim, Kang Yell Choi

Research output: Contribution to journal › Article

22 Citations (Scopus)

Abstract

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/WAF1 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.

Original language	English
Pages (from-to)	27-31
Number of pages	5
Journal	Experimental and Molecular Medicine
Volume	34
Issue number	1
DOIs	https://doi.org/10.1038/emm.2002.4
Publication status	Published - 2002 Mar 31

All Science Journal Classification (ASJC) codes

Biochemistry
Molecular Medicine
Molecular Biology
Clinical Biochemistry

Access to Document

10.1038/emm.2002.4

Fingerprint Dive into the research topics of 'Differential modulation of zinc-stimulated p21<sup>Cip/WAF1</sup> and cyclin D1 induction by inhibition of PI3 kinase in HT-29 colorectal cancer cells'. Together they form a unique fingerprint.

Cite this

Oh, S. Y., Park, K. S., Kim, J. A., & Choi, K. Y. (2002). Differential modulation of zinc-stimulated p21^Cip/WAF1 and cyclin D1 induction by inhibition of PI3 kinase in HT-29 colorectal cancer cells. Experimental and Molecular Medicine, 34(1), 27-31. https://doi.org/10.1038/emm.2002.4

@article{8937bad5027f457fbe8ee91bf893b14c,

title = "Differential modulation of zinc-stimulated p21Cip/WAF1 and cyclin D1 induction by inhibition of PI3 kinase in HT-29 colorectal cancer cells",

abstract = "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 p21Cip/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 p21Cip/WAF1 and cyclin D1. However, in the HT-29 cells pre-treated with PI3K inhibitor, LY294002, zinc induced further the p21Cip/WAF1 induction whereas abrogated cyclin D1 induction. In addition, the induction of p21Cip/WAF1 expression completely inhibited the incorporation of bromodeoxyuridine (BrdU) into the nucleus, indicating that p21Cip/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.",

author = "Oh, {So Young} and Park, {Ki Sook} and Kim, {Jin Ah} and Choi, {Kang Yell}",

year = "2002",

month = mar,

day = "31",

doi = "10.1038/emm.2002.4",

language = "English",

volume = "34",

pages = "27--31",

journal = "Experimental and Molecular Medicine",

issn = "1226-3613",

publisher = "Korean Society of Med. Biochemistry and Mol. Biology",

number = "1",

}

TY - JOUR

T1 - Differential modulation of zinc-stimulated p21Cip/WAF1 and cyclin D1 induction by inhibition of PI3 kinase in HT-29 colorectal cancer cells

AU - Oh, So Young

AU - Park, Ki Sook

AU - Kim, Jin Ah

AU - Choi, Kang Yell

PY - 2002/3/31

Y1 - 2002/3/31

N2 - 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 p21Cip/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 p21Cip/WAF1 and cyclin D1. However, in the HT-29 cells pre-treated with PI3K inhibitor, LY294002, zinc induced further the p21Cip/WAF1 induction whereas abrogated cyclin D1 induction. In addition, the induction of p21Cip/WAF1 expression completely inhibited the incorporation of bromodeoxyuridine (BrdU) into the nucleus, indicating that p21Cip/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.

AB - 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 p21Cip/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 p21Cip/WAF1 and cyclin D1. However, in the HT-29 cells pre-treated with PI3K inhibitor, LY294002, zinc induced further the p21Cip/WAF1 induction whereas abrogated cyclin D1 induction. In addition, the induction of p21Cip/WAF1 expression completely inhibited the incorporation of bromodeoxyuridine (BrdU) into the nucleus, indicating that p21Cip/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.

UR - http://www.scopus.com/inward/record.url?scp=0037204430&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037204430&partnerID=8YFLogxK

U2 - 10.1038/emm.2002.4

DO - 10.1038/emm.2002.4

M3 - Article

C2 - 11989975

AN - SCOPUS:0037204430

VL - 34

SP - 27

EP - 31

JO - Experimental and Molecular Medicine

JF - Experimental and Molecular Medicine

SN - 1226-3613

IS - 1

ER -