Decreased expression of the gut-enriched Kruppel-like factor gene in intestinal adenomas of multiple intestinal neoplasia mice and in colonic adenomas of familial adenomatous polyposis patients

被引:83
作者
Dang, DT
Bachman, KE
Mahatan, CS
Dang, LH
Giardiello, FM
Yang, VW [1 ]
机构
[1] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Sch Med, Grad Program Cellular & Mol Med, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Johns Hopkins Oncol Ctr, Baltimore, MD 21205 USA
[4] Johns Hopkins Univ, Sch Med, Dept Biol Chem, Div Gastroenterol, Baltimore, MD 21205 USA
关键词
gut-enriched Kruppel-like factor; tumorigenesis; Min mouse; familial adenomatous polyposis; reverse transcription-polymerase chain reaction; DNA methylation;
D O I
10.1016/S0014-5793(00)01727-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Gut-enriched Kruppel-like factor (GKLF) is a zinc finger-containing transcription factor, the expression of which is associated with growth arrest. We compared Gklf expression in intestinal and colonic adenomas to normal mucosa in multiple intestinal neoplasia (Min) mice and familiar adenomatous polyposis (FAP) patients, respectively, using semi-quantitative RT-PCR, In Min mice, the level of Gklf transcript is highest in normal-appearing intestinal tissues and decreases as the size of the adenoma increases. In FAP patients, the level of GKLF transcript is lower in adenomas compared to paired normal-appearing mucosa from the same patient or normal colonic mucosa from control individuals without PAP, The possibility of DNA methylation as a cause for the decreased expression of Gklf in adenomas of Min mice was investigated by methylation-specific PCR, Results indicate that the Gklf gene is not methylated in either normal or tumorous tissues. The findings of our study are therefore consistent with the potential role of GKLF as a negative growth regulator of gut epithelial cells. (C) 2000 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:203 / 207
页数:5
相关论文
共 39 条
  • [1] *AM CANC SOC, 1999, CANC FACTS FIG 1999
  • [2] Tying it all together: Epigenetics, genetics, cell cycle, and cancer
    Baylin, SB
    [J]. SCIENCE, 1997, 277 (5334) : 1948 - 1949
  • [3] Homeosis and intestinal tumours in Cdx2 mutant mice
    Chawengsaksophak, K
    James, R
    Hammond, VE
    Kontgen, F
    Beck, F
    [J]. NATURE, 1997, 386 (6620) : 84 - 87
  • [4] CDX2 is mutated in a colorectal cancer with normal APC/β-catenin signaling
    da Costa, LT
    He, TC
    Yu, J
    Sparks, AB
    Morin, PJ
    Polyak, K
    Laken, S
    Vogelstein, B
    Kinzler, KW
    [J]. ONCOGENE, 1999, 18 (35) : 5010 - 5014
  • [5] GENETIC IDENTIFICATION OF MOM-1, A MAJOR MODIFIER LOCUS AFFECTING MIN-INDUCED INTESTINAL NEOPLASIA IN THE MOUSE
    DIETRICH, WF
    LANDER, ES
    SMITH, JS
    MOSER, AR
    GOULD, KA
    LUONGO, C
    BORENSTEIN, N
    DOVE, W
    [J]. CELL, 1993, 75 (04) : 631 - 639
  • [6] EE HC, 1995, AM J PATHOL, V147, P586
  • [7] A GENETIC MODEL FOR COLORECTAL TUMORIGENESIS
    FEARON, ER
    VOGELSTEIN, B
    [J]. CELL, 1990, 61 (05) : 759 - 767
  • [8] FLINT N, 1994, EPITHELIAL CELL BIOL, V3, P16
  • [9] A gene for a novel zinc-finger protein expressed in differentiated epithelial cells and transiently in certain mesenchymal cells
    GarrettSinha, LA
    Eberspaecher, H
    Seldin, MF
    deCrombrugghe, B
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (49) : 31384 - 31390
  • [10] IDENTIFICATION AND CHARACTERIZATION OF THE FAMILIAL ADENOMATOUS POLYPOSIS-COLI GENE
    GRODEN, J
    THLIVERIS, A
    SAMOWITZ, W
    CARLSON, M
    GELBERT, L
    ALBERTSEN, H
    JOSLYN, G
    STEVENS, J
    SPIRIO, L
    ROBERTSON, M
    SARGEANT, L
    KRAPCHO, K
    WOLFF, E
    BURT, R
    HUGHES, JP
    WARRINGTON, J
    MCPHERSON, J
    WASMUTH, J
    LEPASLIER, D
    ABDERRAHIM, H
    COHEN, D
    LEPPERT, M
    WHITE, R
    [J]. CELL, 1991, 66 (03) : 589 - 600