期刊
CLINICAL & EXPERIMENTAL METASTASIS
卷 27, 期 4, 页码 241-249出版社
SPRINGER
DOI: 10.1007/s10585-010-9322-3
关键词
GPR56; Prostate cancer; Breast cancer; Melanoma; Animal models on cancer
类别
资金
- NIH [U54CA126515]
- Virginia and Daniel K Ludwig Fund for Cancer Research
- Howard Hughes Medical Institute
- NATIONAL CANCER INSTITUTE [U54CA126515] Funding Source: NIH RePORTER
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.
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