Transforming growth factor-beta (TGF-β) and brain tumours

被引:32
作者
Luwor, Rodney B. [1 ]
Kaye, Andrew H. [1 ,2 ]
Zhu, Hong-Han [1 ]
机构
[1] Univ Melbourne, Royal Melbourne Hosp, Dept Surg, Parkville, Vic 3050, Australia
[2] Univ Melbourne, Royal Melbourne Hosp, Dept Neurosurg, Parkville, Vic 3050, Australia
关键词
glioma; signalling; TGF-beta; therapy;
D O I
10.1016/j.jocn.2008.01.003
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Since its discovery in the late 1970s considerable research has linked transforming growth factor-beta (TGF-beta) to several human diseases such as fibrosis, auto-immunity and cancer. TGF-beta acts initially as a growth inhibitory factor in early stages of tumour development. In contrast, as tumours evolve, they develop mechanisms to evade the growth-regulatory effects of TGF-beta, resulting in greater tumour invasiveness, increased metastatic potential and inhibition of surrounding immune responses. However, although extensively studied, the molecular mechanisms that trigger tumour cells to "switch" from TGF-beta-inhibited to TGF-beta-promoted are still not fully understood. Contradictory studies that demonstrate opposite cellular effects mediated by TGF-beta are abundant throughout the literature. This review summarizes the current molecular mechanisms involved in the tumour suppressive and tumour progressive characteristics of TGF-beta in brain tumours. Potential therapeutic agents that target TGF-beta and related proteins being evaluated against brain tumours is also discussed. (c) 2008 Elsevier Ltd. All rights reserved.
引用
收藏
页码:845 / 855
页数:11
相关论文
共 110 条
[1]   Induction of inhibitory Smad6 and Smad7 mRNA by TGF-β family members [J].
Afrakhte, M ;
Morén, A ;
Jossan, S ;
Itoh, S ;
Westermark, B ;
Heldin, CH ;
Heldin, NE ;
ten Dijke, P .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1998, 249 (02) :505-511
[2]  
Ashley DM, 1998, CANCER RES, V58, P302
[3]  
Bertone S, 1999, EUR J IMMUNOL, V29, P23, DOI 10.1002/(SICI)1521-4141(199901)29:01<23::AID-IMMU23>3.0.CO
[4]  
2-Y
[5]   Transforming growth factor-β1 mediates epithelial to mesenchymal transdifferentiation through a RhoA-dependent mechanism [J].
Bhowmick, NA ;
Ghiassi, M ;
Bakin, A ;
Aakre, M ;
Lundquist, CA ;
Engel, ME ;
Arteaga, CL ;
Moses, HL .
MOLECULAR BIOLOGY OF THE CELL, 2001, 12 (01) :27-36
[6]   TGFβ:: the molecular Jekyll and Hyde of cancer [J].
Bierie, Brian ;
Moses, Harold L. .
NATURE REVIEWS CANCER, 2006, 6 (07) :506-520
[7]  
Bitzer M, 2000, GENE DEV, V14, P187
[8]  
BODMER S, 1989, J IMMUNOL, V143, P3222
[9]   High TGFβ-Smad activity confers poor prognosis in glioma patients and promotes cell proliferation depending on the methylation of the PDGF-B gene [J].
Bruna, Alejandra ;
Darken, Rachel S. ;
Rojo, Federico ;
Ocana, Alberto ;
Penuelas, Silvia ;
Arias, Alexandra ;
Paris, Raquel ;
Tortosa, Avelina ;
Mora, Jaume ;
Baselga, Jose ;
Seoane, Joan .
CANCER CELL, 2007, 11 (02) :147-160
[10]   Akt promotes cell survival by phosphorylating and inhibiting a forkhead transcription factor [J].
Brunet, A ;
Bonni, A ;
Zigmond, MJ ;
Lin, MZ ;
Juo, P ;
Hu, LS ;
Anderson, MJ ;
Arden, KC ;
Blenis, J ;
Greenberg, ME .
CELL, 1999, 96 (06) :857-868