The Role of GPR55 in Cancer

  • Clara Andradas
  • María M. Caffarel
  • Eduardo Pérez-Gómez
  • Manuel Guzmán
  • Cristina Sánchez
Part of the The Receptors book series (REC, volume 24)


Evidence accumulated during the last few years suggests that GPR55 is an important component of the molecular circuitry that controls cancer cell behavior. As will be described in this chapter, this receptor has been directly or indirectly related to the basic alterations that drive malignant growth: uncontrolled cancer cell proliferation, sustained angiogenesis, and metastatic capability. GPR55 activation promotes cell proliferation, produces pro-angiogenic effects, and favors cancer cell migration. It also modulates immune responses, which may have important implications in the context of cancer pathogenesis as well. In addition, GPR55 is expressed by a large number of human cancer cell lines and human tumors and, most important, its expression correlates with tumor malignancy. Together, these data indicate that GPR55 plays a relevant role in cancer and opens the possibility of considering this orphan receptor as a new therapeutic target and potential biomarker in oncology.


Cancer Cell Proliferation Human Dermal Microvascular Endothelial Cell Human Breast Adenocarcinoma Cell GPR55 Expression GPR55 Agonist 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.



Arachidonoylethanolamide (anandamide)






Cytosolic phospholipase A2


Extracellular signal-regulated kinase


G protein-coupled receptor


Human microvascular endothelial cells


Human umbilical vein endothelial cells




Lysophosphatidic acid




Nuclear factor of activate T-cells


Nerve growth factor


Phosphoinositide 3-kinase


Peroxisome proliferator-activated receptor


Reactive oxygen species


Receptor tyrosine kinase


Short hairpin RNA


Small interference RNA


Transient receptor potential


Vascular endothelial growth factor



This work was supported by grants from Spanish Ministry of Science and Innovation (to CS), Comunidad de Madrid (to MG), Complutense University (to MG), Fundación Mutua Madrileña (to CS), and GW and Otsuka Pharmaceuticals (to CS and MG). CA, MMC, and EP-G were the recipients of research contracts from Spanish Ministry of Science and Innovation, Fundación Ferrer para la Investigación, and Asociación Española Contra el Cáncer, respectively. We are indebted to the members of our laboratory for their continuous support.


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Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  • Clara Andradas
    • 1
  • María M. Caffarel
    • 2
  • Eduardo Pérez-Gómez
    • 1
  • Manuel Guzmán
    • 1
  • Cristina Sánchez
    • 1
  1. 1.Department of Biochemistry and Molecular Biology I, School of BiologyComplutense UniversityMadridSpain
  2. 2.Department of PathologyUniversity of CambridgeCambridgeUK

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