GPR56 Plays Varying Roles in Endogenous Cancer Progression

2011 March 29

Bibliographic Details
Main Authors: Xu, Lei, Begum, Shahinoor, Barry, Marc, Crowley, Denise G., Yang, Liquan, Bronson, Roderick T., Hynes, Richard O.
Other Authors: Koch Institute for Integrative Cancer Research at MIT
Format: Article
Language:en_US
Published: Springer-Verlag 2012
Online Access:http://hdl.handle.net/1721.1/73670
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author Xu, Lei
Begum, Shahinoor
Barry, Marc
Crowley, Denise G.
Yang, Liquan
Bronson, Roderick T.
Hynes, Richard O.
author2 Koch Institute for Integrative Cancer Research at MIT
author_facet Koch Institute for Integrative Cancer Research at MIT
Xu, Lei
Begum, Shahinoor
Barry, Marc
Crowley, Denise G.
Yang, Liquan
Bronson, Roderick T.
Hynes, Richard O.
author_sort Xu, Lei
collection MIT
description 2011 March 29
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spelling mit-1721.1/736702022-09-27T14:01:16Z GPR56 Plays Varying Roles in Endogenous Cancer Progression Xu, Lei Begum, Shahinoor Barry, Marc Crowley, Denise G. Yang, Liquan Bronson, Roderick T. Hynes, Richard O. Koch Institute for Integrative Cancer Research at MIT Xu, Lei Begum, Shahinoor Barry, Marc Crowley, Denise G. 2011 March 29 GPR56, a non-classical adhesion receptor, was previously reported to suppress tumor growth and metastasis in xenograft models using human melanoma cell lines. To understand whether GPR56 plays similar roles in the development of endogenous tumors, we analyzed cancer progression in Gpr56 [superscript −/−] mice using a variety of transgenic cancer models. Our results showed that GPR56 suppressed prostate cancer progression in the TRAMP model on a mixed genetic background, similar to its roles in progression of melanoma xenografts. However, its roles in other cancer types appeared to be complex. It had marginal effects on tumor onset of mammary tumors in the MMTV–PyMT model, but had no effects on subsequent tumor progression in either the MMTV–PyMT mice or the melanoma model, Ink4a/Arf [superscript −/−] tyr-Hras. These results indicate diverse roles of GPR56 in cancer progression and provide the first genetic evidence for the involvement of an adhesion GPCR in endogenous cancer development. 2012-10-09T14:24:07Z 2012-10-09T14:24:07Z 2010-03 2009-10 Article http://purl.org/eprint/type/JournalArticle 0262-0898 1573-7276 http://hdl.handle.net/1721.1/73670 Xu, Lei et al. “GPR56 Plays Varying Roles in Endogenous Cancer Progression.” Clinical & Experimental Metastasis 27.4 (2010): 241–249. en_US http://dx.doi.org/10.1007/s10585-010-9322-3 Clinical and Experimental Metastasis Creative Commons Attribution-Noncommercial-Share Alike 3.0 http://creativecommons.org/licenses/by-nc-sa/3.0/ application/pdf Springer-Verlag PMC
spellingShingle Xu, Lei
Begum, Shahinoor
Barry, Marc
Crowley, Denise G.
Yang, Liquan
Bronson, Roderick T.
Hynes, Richard O.
GPR56 Plays Varying Roles in Endogenous Cancer Progression
title GPR56 Plays Varying Roles in Endogenous Cancer Progression
title_full GPR56 Plays Varying Roles in Endogenous Cancer Progression
title_fullStr GPR56 Plays Varying Roles in Endogenous Cancer Progression
title_full_unstemmed GPR56 Plays Varying Roles in Endogenous Cancer Progression
title_short GPR56 Plays Varying Roles in Endogenous Cancer Progression
title_sort gpr56 plays varying roles in endogenous cancer progression
url http://hdl.handle.net/1721.1/73670
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AT crowleydeniseg gpr56playsvaryingrolesinendogenouscancerprogression
AT yangliquan gpr56playsvaryingrolesinendogenouscancerprogression
AT bronsonroderickt gpr56playsvaryingrolesinendogenouscancerprogression
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