NDLI: PC-1/PrLZ contributes to malignant progression in prostate cancer.

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PC-1/PrLZ contributes to malignant progression in prostate cancer.

Content Provider	Semantic Scholar
Author	Zhang, Hui Bin Wang, Jian Pang, Bo Liang, Rui-Xia Li, Suping Huang, Pei-Tang Wang, Ruoxiang Chung, Leland W. K. Zhau, Haiyen E. Huang, Cuifen Zhou, Jian-Guang
Copyright Year	2007
Abstract	PC-1/PrLZ gene overexpression has been identified to be associated with prostate cancer progression. Previous studies have revealed that PC-1 possesses transforming activity and confers malignant phenotypes to mouse NIH3T3 cells. However, the functional relevance of PC-1 expression changes during prostate cancer development and progression remains to be evaluated. In this study, gain-of-function and loss-of-function analyses in LNCaP and C4-2 cells, respectively, were implemented. Experimental data showed that PC-1 expression was in positive correlation with prostate cancer cell growth and anchor-independent colony formation in vitro, as well as tumorigenicity in athymic BALB/c mice. Moreover, PC-1 expression was also found to promote androgen-independent progression and androgen antagonist Casodex resistance in prostate cancer cells. These results indicate that PC-1 contributes to androgen-independent progression and malignant phenotypes in prostate cancer cells. Furthermore, molecular evidence revealed that PC-1 expression stimulated Akt/protein kinase B signaling pathway, which has been implicated to play important roles in promoting androgen refractory progression in prostate cancer. Increased PC-1 levels in C4-2 cells may represent an adaptive response in prostate cancer, mediating androgen-independent growth and malignant progression. Inhibiting PC-1 expression may represent a novel therapeutic strategy to delay prostate cancer progression.
File Format	PDF HTM / HTML
DOI	10.1158/0008-5472.CAN-06-4214
PubMed reference number	17875733
Journal	Medline
Volume Number	67
Issue Number	18
Alternate Webpage(s)	http://cancerres.aacrjournals.org/content/canres/67/18/8906.full.pdf
Alternate Webpage(s)	https://doi.org/10.1158/0008-5472.CAN-06-4214
Journal	Cancer research
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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