GPR56 plays varying roles in endogenous cancer progression

Lei Xu, Shahinoor Begum, Marc Barry, Denise Crowley, Liquan Yang, Roderick T. Bronson, Richard O. Hynes

Research output: Contribution to journalArticlepeer-review

30 Scopus citations


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.

Original languageEnglish
Pages (from-to)241-249
Number of pages9
JournalClinical and Experimental Metastasis
Issue number4
StatePublished - Apr 2010
Externally publishedYes


  • Animal models on cancer
  • Breast cancer
  • GPR56
  • Melanoma
  • Prostate cancer


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