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 (-/-) 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 (-/-) 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.
journal_name
Clin Exp Metastasisjournal_title
Clinical & experimental metastasisauthors
Xu L,Begum S,Barry M,Crowley D,Yang L,Bronson RT,Hynes ROdoi
10.1007/s10585-010-9322-3subject
Has Abstractpub_date
2010-04-01 00:00:00pages
241-9issue
4eissn
0262-0898issn
1573-7276journal_volume
27pub_type
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更新日期:2012-04-01 00:00:00
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journal_title:Clinical & experimental metastasis
pub_type: 杂志文章
doi:10.1023/a:1015518114931
更新日期:2002-01-01 00:00:00
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journal_title:Clinical & experimental metastasis
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pub_type: 杂志文章,多中心研究
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