TGF-β and cancer

被引：355
作者：
Bierie, B
Moses, HL
机构：
[1] Vanderbilt Univ, Med Ctr, Dept Canc Biol, Nashville, TN USA
[2] Vanderbilt Univ, Med Ctr, Dept Med, Nashville, TN USA
[3] Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Nashville, TN USA
来源：
CYTOKINE & GROWTH FACTOR REVIEWS | 2006年 / 17卷 / 1-2期
关键词：
TGF-beta; Smad; cancer; stroma; epithelium; interactions; cross-talk;
D O I：
10.1016/j.cytogfr.2005.09.006
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：
TGF-beta signaling regulates tumorigenesis and ill human cancer its signaling pathways are often modified during tumor progression. Prior to initiation and early during progression TGF-beta acts upon the epithelium as a tumor Suppressor, however at later stages it is often a tumor promoter. Over the years, many studies have focused on the epithelial cell autonomous role for TGF-beta, however, TGF-beta is not strictly limited to this compartment in vivo. Recent studies addressing TGF-beta mediated stromal-epithelial interactions have significantly improved our understanding related to the regulation of cancer. In addition, stromal fibroblast cell autonomous effects have been observed in response to TGF-beta stimulation. According to the current literature and experimental evidence, TGF-beta is a potent ligand that regulates carcinoma initiation, progression and metastasis through a broad and complex spectrum of interdependent interactions. (c) 2005 Elsevier Ltd. All rights reserved.
引用
收藏
页码：29 / 40
页数：12
相关论文
共 116 条
[1]   TGF-β signaling in cancer -: a double-edged sword [J].
Akhurst, RJ ;
Derynck, R .
TRENDS IN CELL BIOLOGY, 2001, 11 (11) :S44-S51
[2]   Molecular characterization of the tumor microenvironment in breast cancer [J].
Allinen, M ;
Beroukhim, R ;
Cai, L ;
Brennan, C ;
Lahti-Domenici, J ;
Huang, HY ;
Porter, D ;
Hu, M ;
Chin, L ;
Richardson, A ;
Schnitt, S ;
Sellers, WR ;
Polyak, K .
CANCER CELL, 2004, 6 (01) :17-32
[3]   Expression of a dominant negative type II TGF-β receptor in mouse skin results in an increase in carcinoma incidence and an acceleration of carcinoma development [J].
Amendt, C ;
Schirmacher, P ;
Weber, H ;
Blessing, M .
ONCOGENE, 1998, 17 (01) :25-34
[4]  
Anbazhagan R, 1999, CANCER RES, V59, P3363
[5]   Phosphatidylinositol 3-kinase function is required for transforming growth factor β-mediated epithelial to mesenchymal transition and cell migration [J].
Bakin, AV ;
Tomlinson, AK ;
Bhowmick, NA ;
Moses, HL ;
Arteaga, CL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (47) :36803-36810
[6]  
Bakin AV, 2002, J CELL SCI, V115, P3193
[7]  
Bandyopadhyay A, 1999, CANCER RES, V59, P5041
[8]  
Barcellos-Hoff MH, 2000, CANCER RES, V60, P1254
[9]   Higher stromal expression of transforming growth factor-beta type II receptors is associated with poorer prognosis breast tumors [J].
Barlow, J ;
Yandell, D ;
Weaver, D ;
Casey, T ;
Plaut, K .
BREAST CANCER RESEARCH AND TREATMENT, 2003, 79 (02) :149-159
[10]   Increased growth factor production in a human prostatic stromal cell culture model caused by hypoxia [J].
Berger, AP ;
Kofler, K ;
Bektic, J ;
Rogatsch, H ;
Steiner, H ;
Bartsch, G ;
Klocker, H .
PROSTATE, 2003, 57 (01) :57-65
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