More than an accessory: implications of type III transforming growth factor-β receptor loss in prostate cancer

被引：15
|
作者：
Ajiboye, Seun [2 ]
Sissung, Tristan M.
Sharifi, Nima [3 ]
Figg, William D. [1 ,2 ]
机构：
[1] NCI, Clin Pharmacol Program, Med Oncol Clin Res Unit, Med Oncol Branch,Ctr Canc Res, Bethesda, MD 20892 USA
[2] NCI, Mol Pharmacol Sect, Bethesda, MD 20892 USA
[3] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Div Hematol & Oncol, Dallas, TX USA
来源：
BJU INTERNATIONAL | 2010年 / 105卷 / 07期
基金：
美国国家卫生研究院;
关键词：
betaglycan; TGF beta III receptor; prostate cancer; testosterone; TUMOR-SUPPRESSOR; CELL-MIGRATION; BETAGLYCAN; ACTIVINS; INHIBINS; ACTIVATION; EXPRESSION;
D O I：
10.1111/j.1464-410X.2009.08999.x
中图分类号：
R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];
学科分类号：
1002 ; 100201 ;
摘要：
The type III transforming growth factor-beta receptor (TGF beta R3, betaglycan), a tumour suppressor, is the most frequently lost TGF beta pathway component. This event appears to be very important in the transition of the TGF beta pathway from having tumour-suppressor activity in early prostate tumour development, to having tumour-promoting activity in metastatic disease. Moreover, loss of the TGF beta R3 can also affect the cellular response towards testosterone, inhibin/activin, and dysregulate growth-factor pathways that mediate growth and angiogenesis. In this review we discuss how TGF beta R3 normally functions as an accessory protein in the TGF beta pathway, how its loss is related to tumour progression, and the treatment implications of TGF beta R3 loss in individuals with prostate cancer.
引用
收藏
页码：913 / 916
页数：4
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