p21Cip/WAF1 activation is an important factor for the ERK pathway dependent anti-proliferation of colorectal cancer cells

Ki Sook Park, Soung Hoo Jeon, Jong-Won Oh, Kang-Yell Choi

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

p21Cip/WAF1, an important regulator of cell proliferation, is induced by both p53- and extracellular signal regulated kinase (ERK) pathways. The induction of p21Cip/WAF1 occurs by prolonged activation of the ERKs caused by extracellular stimuli, such as zinc. However, not all the cells appeared to respond to ERK pathway dependent p21Cip/WAF1 induction. Here we investigated the cause of such difference using colorectal cancer cells. p21Cip/WAF1 induction and concomitant reduction of bromodeoxyuridine (BrdU) incorporation were observed by zinc treatment within HT-29 and DLD-1. However. HCT-116 cells with high endogenous p21Cip/WAF1 levels did not show any additional increment of p21Cip/WAF1 levels by zinc treatment and did maintain high BrdU incorporation level. The p21 Cip/WAF1 induction by zinc depended upon prolonged activation of extra-cellular signal regulated kinase (ERK) was not observed in HCT-116 cells. The percentage of BrdU positive cells was 50% higher In p21Cip/WAF1 -/ HCT-116 cells compared to p21Cip/WAF1 +/+ HCT-116 cells, and no cells induced p21Cip/WAF1 incorporated BrdU in its nucleus, yet confirming the importance of p21Cip/WAF1 induction in antiproliferation. These results again support that p21Cip/WAF1 induction is a determinant in the regulation of colonic proliferation by the ERK pathway.

Original languageEnglish
Pages (from-to)557-562
Number of pages6
JournalExperimental and Molecular Medicine
Volume36
Issue number6
DOIs
Publication statusPublished - 2004 Dec 31

Fingerprint

HCT116 Cells
Extracellular Signal-Regulated MAP Kinases
Bromodeoxyuridine
Zinc
Colorectal Neoplasms
Chemical activation
Cells
Cell proliferation
Phosphotransferases
Cell Proliferation

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Medicine
  • Molecular Biology
  • Clinical Biochemistry

Cite this

@article{774bfae0582e4bf49c4074936bc014d0,
title = "p21Cip/WAF1 activation is an important factor for the ERK pathway dependent anti-proliferation of colorectal cancer cells",
abstract = "p21Cip/WAF1, an important regulator of cell proliferation, is induced by both p53- and extracellular signal regulated kinase (ERK) pathways. The induction of p21Cip/WAF1 occurs by prolonged activation of the ERKs caused by extracellular stimuli, such as zinc. However, not all the cells appeared to respond to ERK pathway dependent p21Cip/WAF1 induction. Here we investigated the cause of such difference using colorectal cancer cells. p21Cip/WAF1 induction and concomitant reduction of bromodeoxyuridine (BrdU) incorporation were observed by zinc treatment within HT-29 and DLD-1. However. HCT-116 cells with high endogenous p21Cip/WAF1 levels did not show any additional increment of p21Cip/WAF1 levels by zinc treatment and did maintain high BrdU incorporation level. The p21 Cip/WAF1 induction by zinc depended upon prolonged activation of extra-cellular signal regulated kinase (ERK) was not observed in HCT-116 cells. The percentage of BrdU positive cells was 50{\%} higher In p21Cip/WAF1 -/ HCT-116 cells compared to p21Cip/WAF1 +/+ HCT-116 cells, and no cells induced p21Cip/WAF1 incorporated BrdU in its nucleus, yet confirming the importance of p21Cip/WAF1 induction in antiproliferation. These results again support that p21Cip/WAF1 induction is a determinant in the regulation of colonic proliferation by the ERK pathway.",
author = "Park, {Ki Sook} and Jeon, {Soung Hoo} and Jong-Won Oh and Kang-Yell Choi",
year = "2004",
month = "12",
day = "31",
doi = "10.1038/emm.2004.71",
language = "English",
volume = "36",
pages = "557--562",
journal = "Experimental and Molecular Medicine",
issn = "1226-3613",
publisher = "Korean Society of Med. Biochemistry and Mol. Biology",
number = "6",

}

p21Cip/WAF1 activation is an important factor for the ERK pathway dependent anti-proliferation of colorectal cancer cells. / Park, Ki Sook; Jeon, Soung Hoo; Oh, Jong-Won; Choi, Kang-Yell.

In: Experimental and Molecular Medicine, Vol. 36, No. 6, 31.12.2004, p. 557-562.

Research output: Contribution to journalArticle

TY - JOUR

T1 - p21Cip/WAF1 activation is an important factor for the ERK pathway dependent anti-proliferation of colorectal cancer cells

AU - Park, Ki Sook

AU - Jeon, Soung Hoo

AU - Oh, Jong-Won

AU - Choi, Kang-Yell

PY - 2004/12/31

Y1 - 2004/12/31

N2 - p21Cip/WAF1, an important regulator of cell proliferation, is induced by both p53- and extracellular signal regulated kinase (ERK) pathways. The induction of p21Cip/WAF1 occurs by prolonged activation of the ERKs caused by extracellular stimuli, such as zinc. However, not all the cells appeared to respond to ERK pathway dependent p21Cip/WAF1 induction. Here we investigated the cause of such difference using colorectal cancer cells. p21Cip/WAF1 induction and concomitant reduction of bromodeoxyuridine (BrdU) incorporation were observed by zinc treatment within HT-29 and DLD-1. However. HCT-116 cells with high endogenous p21Cip/WAF1 levels did not show any additional increment of p21Cip/WAF1 levels by zinc treatment and did maintain high BrdU incorporation level. The p21 Cip/WAF1 induction by zinc depended upon prolonged activation of extra-cellular signal regulated kinase (ERK) was not observed in HCT-116 cells. The percentage of BrdU positive cells was 50% higher In p21Cip/WAF1 -/ HCT-116 cells compared to p21Cip/WAF1 +/+ HCT-116 cells, and no cells induced p21Cip/WAF1 incorporated BrdU in its nucleus, yet confirming the importance of p21Cip/WAF1 induction in antiproliferation. These results again support that p21Cip/WAF1 induction is a determinant in the regulation of colonic proliferation by the ERK pathway.

AB - p21Cip/WAF1, an important regulator of cell proliferation, is induced by both p53- and extracellular signal regulated kinase (ERK) pathways. The induction of p21Cip/WAF1 occurs by prolonged activation of the ERKs caused by extracellular stimuli, such as zinc. However, not all the cells appeared to respond to ERK pathway dependent p21Cip/WAF1 induction. Here we investigated the cause of such difference using colorectal cancer cells. p21Cip/WAF1 induction and concomitant reduction of bromodeoxyuridine (BrdU) incorporation were observed by zinc treatment within HT-29 and DLD-1. However. HCT-116 cells with high endogenous p21Cip/WAF1 levels did not show any additional increment of p21Cip/WAF1 levels by zinc treatment and did maintain high BrdU incorporation level. The p21 Cip/WAF1 induction by zinc depended upon prolonged activation of extra-cellular signal regulated kinase (ERK) was not observed in HCT-116 cells. The percentage of BrdU positive cells was 50% higher In p21Cip/WAF1 -/ HCT-116 cells compared to p21Cip/WAF1 +/+ HCT-116 cells, and no cells induced p21Cip/WAF1 incorporated BrdU in its nucleus, yet confirming the importance of p21Cip/WAF1 induction in antiproliferation. These results again support that p21Cip/WAF1 induction is a determinant in the regulation of colonic proliferation by the ERK pathway.

UR - http://www.scopus.com/inward/record.url?scp=12344275337&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=12344275337&partnerID=8YFLogxK

U2 - 10.1038/emm.2004.71

DO - 10.1038/emm.2004.71

M3 - Article

VL - 36

SP - 557

EP - 562

JO - Experimental and Molecular Medicine

JF - Experimental and Molecular Medicine

SN - 1226-3613

IS - 6

ER -