Research Paper

Clinical & Experimental Metastasis

, Volume 27, Issue 4, pp 241-249

GPR56 Plays varying roles in endogenous cancer progression

  • Lei XuAffiliated withHoward Hughes Medical Institute and Koch Institute for Integrative Cancer Research, Massachusetts Institute of TechnologyDepartment of Biomedical Genetics, University of Rochester Medical Center Email author 
  • , Shahinoor BegumAffiliated withHoward Hughes Medical Institute and Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
  • , Marc BarryAffiliated withHoward Hughes Medical Institute and Koch Institute for Integrative Cancer Research, Massachusetts Institute of TechnologyDepartment of Pathology, MSC084640, 1 University of New Mexico
  • , Denise CrowleyAffiliated withHoward Hughes Medical Institute and Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
  • , Liquan YangAffiliated withDepartment of Biomedical Genetics, University of Rochester Medical Center
  • , Roderick T. BronsonAffiliated withDepartment of Biomedical Sciences, Tufts University School of Veterinary Medicine
  • , Richard O. HynesAffiliated withHoward Hughes Medical Institute and Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology

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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.

Keywords

GPR56 Prostate cancer Breast cancer Melanoma Animal models on cancer