Stromal-epithelial interaction in prostate cancer progression

被引:57
作者
Chung, Leland W. K.
Huang, Wen-Chin
Sung, Shian-Ying
Wu, Daqing
Odero-Marah, Valerie
Nomura, Takeo
Shigemura, Katsumi
Miyagi, Tohru
Seo, Seogil
Shi, Chumeng
Molitierno, Joe
Elmore, James
Molitierno, Joe
Elmore, James
Anderson, Cynthia
Isotani, Shuji
Edlund, Magnus
Hsieh, Chia-Ling
Wang, Ruoxiang
Shehata, Bahig
Zhau, Haiyen E.
机构
[1] Emory Univ, Sch Med, Dept Urol, Winship Canc Inst, Atlanta, GA 30322 USA
[2] Emory Univ, Sch Med, Dept Urol, Mol Urol & Therapeut Program, Atlanta, GA 30322 USA
关键词
androgen-independent cell; bone metastases; cell signaling; epithelial to mesenchymal transition; extracellular matrices; growth factors; inflammation; osteomimicry; stem cells; tumor stromal interaction;
D O I
10.3816/CGC.2006.n.034
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Cancer is not a single-cell disease, and its existence and behavior are constantly modulated by the host. Cancer gene expression and genetics are also highly dynamic and are regulated epigenetically by the host through gene-environment interaction. In this article, we describe the molecular pathways leading to an unusual property of cancer cells: the ability to mimic the host microenvironment and, in particular, the characteristics of osteomimicry and vasculogenic mimicry, which are likely to be regulated by soluble and insoluble factors in the tumor-adjacent microenvironment. We also discuss the importance of host inflammatory and stem cells that contribute to the growth and survival of cancer cells. By understanding the salient features of cancer-host interaction, novel therapeutics might be developed to target the cancer and its host in the treatment of lethal prostate cancer metastases.
引用
收藏
页码:162 / 170
页数:9
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