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前列腺癌中的 caveolae 形成蛋白 caveolin-1 和 PTRF。

Caveola-forming proteins caveolin-1 and PTRF in prostate cancer.

机构信息

School of Pharmacy, The University of Queensland, 20 Cornwall Street, Woolloongabba, QLD 4102, Australia.

出版信息

Nat Rev Urol. 2013 Sep;10(9):529-36. doi: 10.1038/nrurol.2013.168. Epub 2013 Aug 13.

DOI:10.1038/nrurol.2013.168
PMID:23938946
Abstract

The expression of caveola-forming proteins is dysregulated in prostate cancer. Caveolae are flask-shaped invaginations of the plasma membrane that have roles in membrane trafficking and cell signalling. Members of two families of proteins--caveolins and cavins--are known to be required for the formation and functions of caveolae. Caveolin-1, the major structural protein of caveolae, is overexpresssed in prostate cancer and has been demonstrated to be involved in prostate cancer angiogenesis, growth and metastasis. Polymerase I and transcript release factor (PTRF) is the only cavin family member necessary for caveola formation. When exogenously expressed in prostate cancer cells, PTRF reduces aggressive potential, probably via both caveola-mediated and caveola-independent mechanisms. In addition, stromal PTRF expression decreases with progression of the disease. Evaluation of caveolin-1 antibodies in the clinical setting is underway and it is hoped that future studies will reveal the mechanisms of PTRF action, allowing its targeting for therapeutic purposes.

摘要

小窝形成蛋白的表达在前列腺癌中失调。小窝是质膜的烧瓶状内陷,在膜运输和细胞信号转导中起作用。两种蛋白家族的成员——窖蛋白和窖周蛋白——被认为是小窝形成和功能所必需的。小窝的主要结构蛋白窖蛋白-1在前列腺癌中过度表达,并已被证明参与前列腺癌血管生成、生长和转移。聚合酶 I 和转录释放因子(PTRF)是形成小窝所必需的唯一窖周蛋白家族成员。当外源性表达于前列腺癌细胞中时,PTRF 通过小窝介导和非小窝依赖机制降低侵袭潜能。此外,随着疾病的进展,基质 PTRF 的表达减少。目前正在临床环境中评估窖蛋白-1 抗体,希望未来的研究将揭示 PTRF 作用的机制,从而使其成为治疗的靶点。

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