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|Title:||Prostate cancer cells modulate osteoblast mineralisation and osteoclast differentiation through Id-1|
|Authors:||Wong, YC;Chan, KW;Yuen, HF;Chiu, YT;Chan, KK;Chan, YP;Chua, CW;McCrudden, CM;Tang, KH;ElTanani, M;Wang, X|
|subject:||Bone metastasis;Id-1;Osteoblast;Osteoclast;Prostate Cancer|
|Publisher:||Nature Publishing Group. The Journal's web site is located at http://www.nature.com/bjc|
|Description:||Background: Id-1 is overexpressed in and correlated with metastatic potential of prostate cancer. The role of Id-1 in this metastatic process was further analysed. Methods: Conditioned media from prostate cancer cells, expressing various levels of Id-1, were used to stimulate pre-osteoclast differentiation and osteoblast mineralisation. Downstream effectors of Id-1 were identified. Expressions of Id-1 and its downstream effectors in prostate cancers were studied using immunohistochemistry in a prostate cancer patient cohort (N110). Results: We found that conditioned media from LNCaP prostate cancer cells overexpressing Id-1 had a higher ability to drive osteoclast differentiation and a lower ability to stimulate osteoblast mineralisation than control, whereas conditioned media from PC3 prostate cancer cells with Id-1 knockdown were less able to stimulate osteoclast differentiation. Id-1 was found to negatively regulate TNF-Β and this correlation was confirmed in human prostate cancer specimens (P0.03). Furthermore, addition of recombinant TNF-Β to LNCaP Id-1 cell-derived media blocked the effect of Id-1 overexpression on osteoblast mineralisation. Conclusion: In prostate cancer cells, the ability of Id-1 to modulate bone cell differentiation favouring metastatic bone disease is partially mediated by TNF-Β, and Id-1 could be a potential therapeutic target for prostate cancer to bone metastasis. © 2010 Cancer Research UK. All rights reserved.|
|Standard no:||British Journal Of Cancer, 2010, v. 102 n. 2, p. 332-341|
|Appears in Collections:||Department of Anatomy|
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