The Tale of Transforming Growth Factor-Beta (TGFβ) Signaling: A Soigne Enigma

被引：80

作者：

Chaudhury, Arindam ^{[1
,2
]}

Howe, Philip H. ^{[1
,2
]}

机构：

[1] Cleveland Clin, Lerner Res Inst, Dept Canc Biol, Cleveland, OH 44195 USA

[2] Cleveland State Univ, Dept Biol Geol & Environm Sci, Cleveland, OH 44115 USA

来源：

IUBMB LIFE | 2009年 / 61卷 / 10期

关键词：

transforming growth factor-beta (TGF beta); TGF beta receptors; Smads; canonical signaling; non-canonical signaling; carcinogenesis; cytostatic effects; epithelial to mesenchymal transition (EMT); EPITHELIAL-MESENCHYMAL TRANSITION; ACTIVATED PROTEIN-KINASE; WEHI-231; B-LYMPHOCYTES; NON-NEOPLASTIC TISSUES; COLON CARCINOMA-CELLS; FYVE DOMAIN PROTEIN; C-MYC; SMAD PATHWAY; HA-RAS; (TGF-BETA)-INDUCED APOPTOSIS;

D O I：

10.1002/iub.239

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Transforming growth factor-beta (TGF beta) is a secreted cytokine, which intricately controls a plethora of physiological and pathological processes during development and carcinogenesis. TGF beta exerts antiproliferative effects and functions as a tumor suppressor during early stages of tumorigenesis, whereas at later stages it functions as a tumor promoter aiding in metastatic progression through an autocrine TGF beta loop. Intricate knowledge of TGF beta signaling and its regulation are still evolving. In this review, we make an attempt to showcase the associated enigma of TGF beta signaling in its dual functional role as tumor suppressor and metastatic promoter during early and late stages of carcinogenesis, respectively. (C) 2009 IUBMB IUBMB Life, 61(10): 929-939, 2009

引用

页码：929 / 939

页数：11

共 156 条

[1]

A Mutant-p53/Smad Complex Opposes p63 to Empower TGFβ-Induced Metastasis [J].