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前列腺癌中的基质-上皮细胞相互作用

Stroma-epithelium crosstalk in prostate cancer.

作者信息

Niu Yi-Nong, Xia Shu-Jie

机构信息

Department of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.

出版信息

Asian J Androl. 2009 Jan;11(1):28-35. doi: 10.1038/aja.2008.39. Epub 2008 Dec 22.

DOI:10.1038/aja.2008.39
PMID:19098934
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3735213/
Abstract

The critical role played by stroma-epithelium crosstalk in carcinogenesis and progression of prostate cancer has been increasingly recognized. These interactions are mediated by a variety of paracrine factors secreted by cancer cells and/or stromal cells. In human prostate cancer, reactive stroma is characterized by an increase in myofibroblasts and a corresponding amplification of extracellular matrix production and angiogenesis. Permanent genetic mutations have been reported in stromal cells as well as in tumour cells. Transforming growth factor-beta, vascular endothelial growth factor, platelet-derived growth factor and fibroblast growth factor signalling pathways are involved in the process of angiogenesis, whereas hepatocyte growth factor, insulin-like growth factor-1, epidermal growth factor, CXC12 and Interleukin-6 play active roles in the progression, androgen-independent conversion and distal metastasis of prostate cancer. Some soluble factors have reciprocal interactions with androgens and the androgen receptor (AR), and can even activate AR in the absence of the androgen ligand. In this article, we review the complex interactions between cancer cells and the surrounding microenvironment, and discuss the potential therapeutic targets in the stromal compartment of prostate cancer.

摘要

基质-上皮细胞相互作用在前列腺癌发生和进展中所起的关键作用已得到越来越多的认可。这些相互作用由癌细胞和/或基质细胞分泌的多种旁分泌因子介导。在人类前列腺癌中,反应性基质的特征是肌成纤维细胞增加以及细胞外基质产生和血管生成相应增强。基质细胞以及肿瘤细胞中均已报道存在永久性基因突变。转化生长因子-β、血管内皮生长因子、血小板衍生生长因子和成纤维细胞生长因子信号通路参与血管生成过程,而肝细胞生长因子、胰岛素样生长因子-1、表皮生长因子、CXC12和白细胞介素-6在前列腺癌的进展、雄激素非依赖性转化和远处转移中发挥积极作用。一些可溶性因子与雄激素和雄激素受体(AR)存在相互作用,甚至在没有雄激素配体的情况下也能激活AR。在本文中,我们综述了癌细胞与周围微环境之间的复杂相互作用,并讨论了前列腺癌基质区室中的潜在治疗靶点。

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本文引用的文献

1
Androgenic control of transforming growth factor-beta signaling in prostate epithelial cells through transcriptional suppression of transforming growth factor-beta receptor II.通过转录抑制转化生长因子-β受体II实现雄激素对前列腺上皮细胞中转化生长因子-β信号传导的调控。
Cancer Res. 2008 Oct 1;68(19):8173-82. doi: 10.1158/0008-5472.CAN-08-2290.
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Human prostate stromal cells stimulate increased PSA production in DHEA-treated prostate cancer epithelial cells.人前列腺基质细胞刺激经脱氢表雄酮处理的前列腺癌上皮细胞中前列腺特异性抗原产量增加。
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Role of IGF-1/IGF-1R in regulation of invasion in DU145 prostate cancer cells.IGF-1/IGF-1R在DU145前列腺癌细胞侵袭调控中的作用。
Cancer Cell Int. 2008 Jul 3;8:10. doi: 10.1186/1475-2867-8-10.
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Targeting the c-MET signaling pathway for cancer therapy.以c-MET信号通路为靶点进行癌症治疗。
Expert Opin Investig Drugs. 2008 Jul;17(7):997-1011. doi: 10.1517/13543784.17.7.997.
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Platelet-derived growth factor-D overexpression contributes to epithelial-mesenchymal transition of PC3 prostate cancer cells.血小板衍生生长因子-D的过表达促进了PC3前列腺癌细胞的上皮-间质转化。
Stem Cells. 2008 Jun;26(6):1425-35. doi: 10.1634/stemcells.2007-1076. Epub 2008 Apr 10.
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Androgen receptor signalling in prostate: effects of stromal factors on normal and cancer stem cells.前列腺中的雄激素受体信号传导:基质因子对正常和癌症干细胞的影响。
Mol Cell Endocrinol. 2008 Jun 25;288(1-2):30-7. doi: 10.1016/j.mce.2008.02.024. Epub 2008 Mar 2.
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HGF/SF up-regulates the expression of bone morphogenetic protein 7 in prostate cancer cells.肝细胞生长因子/散射因子上调前列腺癌细胞中骨形态发生蛋白7的表达。
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