Differential effect of NF-κB activity on β-catenin/Tcf pathway in various cancer cells

被引：60

作者：

Cho, Hyun Hwa ^{[1
]}

Song, Ji Sun ^{[1
]}

Yu, Ji Min ^{[1
,2
]}

Yu, Sung Sook ^{[1
,4
]}

Choi, Sung Jong ^{[5
]}

Kim, Dong Heon ^{[6
]}

Jung, Jin Sup ^{[1
,2
,3
]}

机构：

[1] Pusan Natl Univ, Dept Physiol, Sch Med, Pusan 602739, South Korea

[2] Pusan Natl Univ, Med Res Ctr Ischem Tissue Regenerat, Pusan 602739, South Korea

[3] Pusan Natl Univ, Med Res Inst, Pusan 602739, South Korea

[4] Pusan Natl Univ, BK21 Med Sci Educ Ctr, Sch Med, Pusan 602739, South Korea

[5] Pusan Med Ctr, Pusan, South Korea

[6] Pusan Natl Univ, Dept Surg, Sch Med, Pusan 602739, South Korea

来源：

FEBS LETTERS | 2008年 / 582卷 / 05期

基金：

英国医学研究理事会;

关键词：

cancer cell; beta-catenin/Tcf; NF-kappa B; lucine zipper tumor suppressor 2;

D O I：

10.1016/j.febslet.2008.01.029

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

beta-Catenin/Tcf and NF-kappa B pathways play an important role in biological functions. We determined the underlying mechanisms of differential interaction between two pathways in various human cancer cell lines. NF-kappa B positively regulated beta-catenin/Tcf pathways in human glioblastoma, whereas it has an opposite effect on beta-catenin/Tcf pathways in colon, liver, and breast cancer cells. Expression of lucine zipper tumor suppressor 2 (lzts2) was positively regulated by NF-kappa B activity in colon, liver, and breast cancer cells, whereas negatively regulated in glioma cells. Downregulation of lzts2 increased the beta-catenin/Tcf promoter activity and inhibited NF-kappa B-induced modulation of the nuclear translocation of beta-catenin. These data indicate that the differential crosstalk between beta-catenin/Tcf and NF-kappa B pathway in various cancer cells is resulted from the differences in the regulation of NF-kappa B-induced lzts2 expression. (C) 2008 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：616 / 622

页数：7

共 26 条

[1]

dlk1/FA1 regulates the function of human bone marrow mesenchymal stem cells by modulating gene expression of pro-inflammatory cytokines and immune response-related factors [J].