TGFβ signalling: a complex web in cancer progression

被引:915
作者
Ikushima, Hiroaki [1 ]
Miyazono, Kohei [1 ]
机构
[1] Univ Tokyo, Dept Mol Pathol, Grad Sch Med, Tokyo 1130033, Japan
关键词
GROWTH-FACTOR-BETA; EPITHELIAL-MESENCHYMAL TRANSITIONS; RECEPTOR KINASE INHIBITOR; TRANSCRIPTION FACTOR DEC1; HORMONE-RELATED PROTEIN; PROMOTES TUMOR-GROWTH; NON-HODGKINS-LYMPHOMA; BREAST-CANCER; STEM-CELLS; TRANSFORMING GROWTH-FACTOR-BETA-1;
D O I
10.1038/nrc2853
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The distortion of growth factor signalling is the most important prerequisite in tumour progression. Transforming growth factor-beta (TGF beta) signalling regulates tumour progression by a tumour cell-autonomous mechanism or through tumour-stroma interaction, and has either a tumour-suppressing or tumour-promoting function depending on cellular context. Such inherent complexity of TGF beta signalling results in arduous, but promising, assignments for developing therapeutic strategies against malignant tumours. As numerous cellular context-dependent factors tightly maintain the balance of TGF beta signalling and contribute to the regulation of TGF beta-induced cell responses, in this Review we discuss how they maintain the balance of TGF beta signalling and how their collapse leads to tumour progression.
引用
收藏
页码:415 / 424
页数:10
相关论文
共 131 条
[21]   Ski and SnoN, potent negative regulators of TGF-β signaling [J].
Deheuninck, Julien ;
Luo, Kunxin .
CELL RESEARCH, 2009, 19 (01) :47-57
[22]   TGF-β signaling in tumor suppression and cancer progression [J].
Derynck, R ;
Akhurst, RJ ;
Balmain, A .
NATURE GENETICS, 2001, 29 (02) :117-129
[23]   Smad-dependent and Smad-independent pathways in TGF-β family signalling [J].
Derynck, R ;
Zhang, YE .
NATURE, 2003, 425 (6958) :577-584
[24]   Bim is a suppressor of Myc-induced mouse B cell leukemia [J].
Egle, A ;
Harris, AW ;
Bouillet, P ;
Cory, S .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (16) :6164-6169
[25]   Transforming growth factor-β promotes survival of mammary carcinoma cells through induction of antiapoptotic transcription factor DEC1 [J].
Ehata, Shogo ;
Hanyu, Aki ;
Hayashi, Makoto ;
Aburatani, Hiroyuki ;
Kato, Yukio ;
Fujime, Makoto ;
Saitoh, Masao ;
Miyazawa, Keiji ;
Imamura, Takeshi ;
Miyazono, Kohei .
CANCER RESEARCH, 2007, 67 (20) :9694-9703
[26]   Ki26894, a novel transforming growth factor-β type I receptor kinase inhibitor, inhibits in vitro invasion and in vivo bone metastasis of a human breast cancer cell line [J].
Ehata, Shogo ;
Hanyu, Aki ;
Fujime, Makoto ;
Katsuno, Yoko ;
Fukunaga, Erina ;
Goto, Kouichiro ;
Ishikawa, Yuichi ;
Nomura, Kimie ;
Yokoo, Hiroshi ;
Shimizu, Toshiyuki ;
Ogata, Etsuro ;
Miyazono, Kohei ;
Shimizu, Kiyoshi ;
Imamura, Takeshi .
CANCER SCIENCE, 2007, 98 (01) :127-133
[27]   The paradox of autophagy and its implication in cancer etiology and therapy [J].
Eisenberg-Lerner, Avital ;
Kimchi, Adi .
APOPTOSIS, 2009, 14 (04) :376-391
[28]   The tumor suppressor Smad4/DPC4 and transcriptional adaptor CBP/p300 are coactivators for Smad3 in TGF-β-induced transcriptional activation [J].
Feng, XH ;
Zhang, Y ;
Wu, RY ;
Derynck, R .
GENES & DEVELOPMENT, 1998, 12 (14) :2153-2163
[29]   Specificity and versatility in TGF-β signaling through Smads [J].
Feng, XH ;
Derynck, R .
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, 2005, 21 :659-693
[30]   Sox2 deficiency causes neurodegeneration and impaired neurogenesis in the adult mouse brain [J].
Ferri, ALM ;
Cavallaro, M ;
Braida, D ;
Di Cristofano, A ;
Canta, A ;
Vezzani, A ;
Ottolenghi, S ;
Pandolfi, PP ;
Sala, M ;
DeBiasi, S ;
Nicolis, SK .
DEVELOPMENT, 2004, 131 (15) :3805-3819