GPR56 Plays Varying Roles in Endogenous Cancer Progression
Name
Hynes_GPR56 plays.pdf
Size
991.9 KB
Format
Adobe PDF
Checksum (MD5)
8039e1273ae3c4780b2b177b79ada3fb
Author(s) • • • • • •
Xu, Lei
Begum, Shahinoor
Barry, Marc
Crowley, Denise G.
Yang, Liquan
Bronson, Roderick T.
Hynes, Richard O.
Date Issued
March 2010
Journal
Clinical and Experimental Metastasis
Publisher
Springer-Verlag
Citation
Xu, Lei et al. “GPR56 Plays Varying Roles in Endogenous Cancer Progression.” Clinical & Experimental Metastasis 27.4 (2010): 241–249.
Version
Author's final manuscript
Abstract
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.
Description
2011 March 29
MIT Department
Koch Institute for Integrative Cancer Research at MIT
Terms of Use
Creative Commons Attribution-Noncommercial-Share Alike 3.0
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1007/s10585-010-9322-3