Clinical & Experimental Metastasis

, Volume 27, Issue 4, pp 241–249

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 Paper

DOI: 10.1007/s10585-010-9322-3

Cite this article as:
Xu, L., Begum, S., Barry, M. et al. Clin Exp Metastasis (2010) 27: 241. doi:10.1007/s10585-010-9322-3

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

GPR56Prostate cancerBreast cancerMelanomaAnimal models on cancer

Abbreviations

BFPP

Bilateral frontoparietal polymicrogyria

ECM

Extracellular matrix

GPCR

G protein-coupled receptor

GPR56

G protein-coupled receptor 56

MMTV

Mouse mammary tumor virus

PyMT

Polyoma middle T oncogene

RIPA

Radio-immunoprecipitation assay

TG2

Tissue transglutaminase

TRAMP

Transgenic adenocarcinoma of the mouse prostate

Supplementary material

10585_2010_9322_MOESM1_ESM.pdf (293 kb)
Supplementary material 1 (PDF 292 kb)

Copyright information

© Springer Science+Business Media B.V. 2010

Authors and Affiliations

  • Lei Xu
    • 1
    • 3
  • Shahinoor Begum
    • 1
  • Marc Barry
    • 1
    • 4
  • Denise Crowley
    • 1
  • Liquan Yang
    • 3
  • Roderick T. Bronson
    • 2
  • Richard O. Hynes
    • 1
  1. 1.Howard Hughes Medical Institute and Koch Institute for Integrative Cancer ResearchMassachusetts Institute of TechnologyCambridgeUSA
  2. 2.Department of Biomedical SciencesTufts University School of Veterinary MedicineNorth GraftonUSA
  3. 3.Department of Biomedical GeneticsUniversity of Rochester Medical CenterRochesterUSA
  4. 4.Department of Pathology, MSC0846401 University of New MexicoAlbuquerqueUSA