Differential regulation of MAP kinase cascade in human colorectal tumorigenesis

K. S. Park, N. G. Kim, J. J. Kim, H. Kim, Y. H. Ahn, Kang-Yell Choi

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Hyper-activation of mitogen-activated protein kinase (MAPK) has recently been reported in several human cancers and activation of MAPK in those cancers may be associated with carcinogenesis through aberrant cell proliferation. To understand the roles of the MARK pathway in colorectal tumorigenesis, we examined the status of extracellular signal-regulated protein kinases (ERK1/2) in 21 colorectal tumour specimens and compared it with that of paired normals. The specific MAPK activities were two- to tenfold lower in 71% (15 out of 21 cases) of colorectal tumours compared to those in paired normals. The individual MAPK kinase (MEK) correlated with MARK activities (P = 0.006). Reduction of the MAPK and MEK activities in colorectal tumours was also observed in adenomas. These results suggested that down-regulation of the MAPK cascade may be caused by early genetic event(s) and that it may be related to the loss of normal growth control. Although MAPK activities were down-regulated both in adenomas and carcinomas, activities of the MAPKs in carcinomas were higher than those of paired adenomas. These results suggested that MARK activities may be increased in the adenoma-to-carcinoma sequence and that it may play a role in the tumour progression. Observation of the differential regulation of MAPK activities in colorectal tumorigeneis suggested roles for the MAPK pathway in both positive and negative controls of cell growth.

Original languageEnglish
Pages (from-to)1116-1121
Number of pages6
JournalBritish Journal of Cancer
Volume81
Issue number7
DOIs
Publication statusPublished - 1999 Jan 1

Fingerprint

MAP Kinase Signaling System
Mitogen-Activated Protein Kinases
Carcinogenesis
Adenoma
Mitogen-Activated Protein Kinase Kinases
Colorectal Neoplasms
Carcinoma
Neoplasms
Extracellular Signal-Regulated MAP Kinases
Growth
Protein Kinases
Down-Regulation
Cell Proliferation
Observation

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Park, K. S. ; Kim, N. G. ; Kim, J. J. ; Kim, H. ; Ahn, Y. H. ; Choi, Kang-Yell. / Differential regulation of MAP kinase cascade in human colorectal tumorigenesis. In: British Journal of Cancer. 1999 ; Vol. 81, No. 7. pp. 1116-1121.
@article{65be2c73de814f72a913228635b1d7ae,
title = "Differential regulation of MAP kinase cascade in human colorectal tumorigenesis",
abstract = "Hyper-activation of mitogen-activated protein kinase (MAPK) has recently been reported in several human cancers and activation of MAPK in those cancers may be associated with carcinogenesis through aberrant cell proliferation. To understand the roles of the MARK pathway in colorectal tumorigenesis, we examined the status of extracellular signal-regulated protein kinases (ERK1/2) in 21 colorectal tumour specimens and compared it with that of paired normals. The specific MAPK activities were two- to tenfold lower in 71{\%} (15 out of 21 cases) of colorectal tumours compared to those in paired normals. The individual MAPK kinase (MEK) correlated with MARK activities (P = 0.006). Reduction of the MAPK and MEK activities in colorectal tumours was also observed in adenomas. These results suggested that down-regulation of the MAPK cascade may be caused by early genetic event(s) and that it may be related to the loss of normal growth control. Although MAPK activities were down-regulated both in adenomas and carcinomas, activities of the MAPKs in carcinomas were higher than those of paired adenomas. These results suggested that MARK activities may be increased in the adenoma-to-carcinoma sequence and that it may play a role in the tumour progression. Observation of the differential regulation of MAPK activities in colorectal tumorigeneis suggested roles for the MAPK pathway in both positive and negative controls of cell growth.",
author = "Park, {K. S.} and Kim, {N. G.} and Kim, {J. J.} and H. Kim and Ahn, {Y. H.} and Kang-Yell Choi",
year = "1999",
month = "1",
day = "1",
doi = "10.1038/sj.bjc.6690817",
language = "English",
volume = "81",
pages = "1116--1121",
journal = "British Journal of Cancer",
issn = "0007-0920",
publisher = "Nature Publishing Group",
number = "7",

}

Differential regulation of MAP kinase cascade in human colorectal tumorigenesis. / Park, K. S.; Kim, N. G.; Kim, J. J.; Kim, H.; Ahn, Y. H.; Choi, Kang-Yell.

In: British Journal of Cancer, Vol. 81, No. 7, 01.01.1999, p. 1116-1121.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Differential regulation of MAP kinase cascade in human colorectal tumorigenesis

AU - Park, K. S.

AU - Kim, N. G.

AU - Kim, J. J.

AU - Kim, H.

AU - Ahn, Y. H.

AU - Choi, Kang-Yell

PY - 1999/1/1

Y1 - 1999/1/1

N2 - Hyper-activation of mitogen-activated protein kinase (MAPK) has recently been reported in several human cancers and activation of MAPK in those cancers may be associated with carcinogenesis through aberrant cell proliferation. To understand the roles of the MARK pathway in colorectal tumorigenesis, we examined the status of extracellular signal-regulated protein kinases (ERK1/2) in 21 colorectal tumour specimens and compared it with that of paired normals. The specific MAPK activities were two- to tenfold lower in 71% (15 out of 21 cases) of colorectal tumours compared to those in paired normals. The individual MAPK kinase (MEK) correlated with MARK activities (P = 0.006). Reduction of the MAPK and MEK activities in colorectal tumours was also observed in adenomas. These results suggested that down-regulation of the MAPK cascade may be caused by early genetic event(s) and that it may be related to the loss of normal growth control. Although MAPK activities were down-regulated both in adenomas and carcinomas, activities of the MAPKs in carcinomas were higher than those of paired adenomas. These results suggested that MARK activities may be increased in the adenoma-to-carcinoma sequence and that it may play a role in the tumour progression. Observation of the differential regulation of MAPK activities in colorectal tumorigeneis suggested roles for the MAPK pathway in both positive and negative controls of cell growth.

AB - Hyper-activation of mitogen-activated protein kinase (MAPK) has recently been reported in several human cancers and activation of MAPK in those cancers may be associated with carcinogenesis through aberrant cell proliferation. To understand the roles of the MARK pathway in colorectal tumorigenesis, we examined the status of extracellular signal-regulated protein kinases (ERK1/2) in 21 colorectal tumour specimens and compared it with that of paired normals. The specific MAPK activities were two- to tenfold lower in 71% (15 out of 21 cases) of colorectal tumours compared to those in paired normals. The individual MAPK kinase (MEK) correlated with MARK activities (P = 0.006). Reduction of the MAPK and MEK activities in colorectal tumours was also observed in adenomas. These results suggested that down-regulation of the MAPK cascade may be caused by early genetic event(s) and that it may be related to the loss of normal growth control. Although MAPK activities were down-regulated both in adenomas and carcinomas, activities of the MAPKs in carcinomas were higher than those of paired adenomas. These results suggested that MARK activities may be increased in the adenoma-to-carcinoma sequence and that it may play a role in the tumour progression. Observation of the differential regulation of MAPK activities in colorectal tumorigeneis suggested roles for the MAPK pathway in both positive and negative controls of cell growth.

UR - http://www.scopus.com/inward/record.url?scp=0032754892&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032754892&partnerID=8YFLogxK

U2 - 10.1038/sj.bjc.6690817

DO - 10.1038/sj.bjc.6690817

M3 - Article

C2 - 10584870

AN - SCOPUS:0032754892

VL - 81

SP - 1116

EP - 1121

JO - British Journal of Cancer

JF - British Journal of Cancer

SN - 0007-0920

IS - 7

ER -