TGF-β: Duality of Function Between Tumor Prevention and Carcinogenesis

被引：413

作者：

Principe, Daniel R. ^{[1
,3
,5
]}

Doll, Jennifer A. ^{[6
]}

Bauer, Jessica ^{[1
]}

Jung, Barbara ^{[1
]}

Munshi, Hidayatullah G. ^{[2
]}

Bartholin, Laurent ^{[7
]}

Pasche, Boris ^{[8
]}

Lee, Chung ^{[4
,9
]}

Grippo, Paul J. ^{[3
]}

机构：

[1] Northwestern Univ Feinberg Sch Med, Dept Med, Div Gastroenterol, Chicago, IL 60611 USA

[2] Northwestern Univ Feinberg Sch Med, Div Hematol Oncol, Chicago, IL 60611 USA

[3] Northwestern Univ Feinberg Sch Med, Dept Surg, Div GI Surg Oncol, Chicago, IL 60611 USA

[4] Northwestern Univ Feinberg Sch Med, Dept Urol, Chicago, IL 60611 USA

[5] Northwestern Univ, Dept Biomed Engn, McCormick Sch Engn, Evanston, IL 60208 USA

[6] Univ Wisconsin, Dept Biomed Sci, Milwaukee, WI 53201 USA

[7] Univ Lyon 1, Ctr Rech Cancerol Lyon, UMR INSERM U1052, CNRS 5286, F-69365 Lyon, France

[8] Univ Alabama Birmingham, Dept Med, Div Hematol Oncol, Birmingham, AL 35294 USA

[9] Univ Calif Irvine, Dept Pathol & Lab Med, Irvine, CA USA

来源：

JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE | 2014年 / 106卷 / 02期

关键词：

GROWTH-FACTOR-BETA; REGULATORY T-CELLS; EPITHELIAL-MESENCHYMAL TRANSITION; PROSTATE-CANCER CELLS; TRANSFORMING GROWTH-FACTOR-BETA-1; PANCREATIC-CANCER; E-CADHERIN; EXTRACELLULAR-MATRIX; ADOPTIVE TRANSFER; TRANSGENIC MICE;

D O I：

10.1093/jnci/djt369

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Several mechanisms underlying tumor progression have remained elusive, particularly in relation to transforming growth factor beta (TGF-beta). Although TGF-beta initially inhibits epithelial growth, it appears to promote the progression of advanced tumors. Defects in normal TGF-beta pathways partially explain this paradox, which can lead to a cascade of downstream events that drive multiple oncogenic pathways, manifesting as several key features of tumorigenesis (uncontrolled proliferation, loss of apoptosis, epithelial-to-mesenchymal transition, sustained angiogenesis, evasion of immune surveillance, and metastasis). Understanding the mechanisms of TGF-beta dysregulation will likely reveal novel points of convergence between TGF-beta and other pathways that can be specifically targeted for therapy.

引用

页数：16

共 203 条

[1] Tgfbr1 Haploinsufficiency Inhibits the Development of Murine Mutant Kras-Induced Pancreatic Precancer [J].

Adrian, Kevin ;

Strouch, Matthew J. ;

Zeng, Qinghua ;

Barron, Morgan R. ;

Cheon, Eric C. ;

Honasoge, Akilesh ;

Xu, Yanfei ;

Phukan, Sharbani ;

Sadim, Maureen ;

Bentrem, David J. ;

Pasche, Boris ;

Grippo, Paul J. .

CANCER RESEARCH, 2009, 69 (24) :9169-9174

[2] Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma [J].

Aguirre, AJ ;

Bardeesy, N ;

Sinha, M ;

Lopez, L ;

Tuveson, DA ;

Horner, J ;

Redston, MS ;

DePinho, RA .

GENES & DEVELOPMENT, 2003, 17 (24) :3112-3126

[3] TGF-β signaling in cancer -: a double-edged sword [J].

Akhurst, RJ ;

Derynck, R .

TRENDS IN CELL BIOLOGY, 2001, 11 (11) :S44-S51

[4] 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

[5] Making sense of latent TGFβ activation [J].

Annes, JP ;

Munger, JS ;

Rifkin, DB .

JOURNAL OF CELL SCIENCE, 2003, 116 (02) :217-224

[6] Smad7 abrogates transforming growth factor-β1-mediated growth inhibition in COLO-357 cells through functional inactivation of the retinoblastoma protein [J].

Arnold, NB ;

Korc, M .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (23) :21858-21866

[7] 4E-BP1 is a target of Smad4 essential for TGFβ-mediated inhibition of cell proliferation [J].

Azar, Rania ;

Alard, Amandine ;

Susini, Christiane ;

Bousquet, Corinne ;

Pyronnet, Stephane .

EMBO JOURNAL, 2009, 28 (22) :3514-3522

[8] Redox-mediated activation of latent transforming growth factor-beta 1 [J].

BarcellosHoff, MH ;

Dix, TA .

MOLECULAR ENDOCRINOLOGY, 1996, 10 (09) :1077-1083

[9] Smad4 is dispensable for normal pancreas development yet critical in progression and tumor biology of pancreas cancer [J].

Bardeesy, Nabeel ;

Cheng, Kuang-hung ;

Berger, Justin H. ;

Chu, Gerald C. ;

Pahler, Jessica ;

Olson, Peter ;

Hezel, Aram F. ;

Horner, James ;

Lauwers, Gregory Y. ;

Hanahan, Douglas ;

DePinho, Ronald A. .

GENES & DEVELOPMENT, 2006, 20 (22) :3130-3146

[10] Identification of PP2A as a crucial regulator of the NF-κB feedback loop: its inhibition by UVB turns NF-κB into a pro-apoptotic factor [J].

Barisic, S. ;

Strozyk, E. ;

Peters, N. ;

Walczak, H. ;

Kulms, D. .

CELL DEATH AND DIFFERENTIATION, 2008, 15 (11) :1681-1690

← 1 2 3 4 5 6 7 8 9 10 →