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The Role of GPR55 in Cancer

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endoCANNABINOIDS

Part of the book series: The Receptors ((REC,volume 24))

Abstract

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.

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Abbreviations

AEA:

Arachidonoylethanolamide (anandamide)

CBD:

Cannabidiol

COX-2:

Cyclooxygenase-2

cPLA2:

Cytosolic phospholipase A2

ERK:

Extracellular signal-regulated kinase

GPCR:

G protein-coupled receptor

HMVEC:

Human microvascular endothelial cells

HUVEC:

Human umbilical vein endothelial cells

LOX:

Lipoxygenase

LPA:

Lysophosphatidic acid

LPI:

Lysophosphatidylinositol

NFAT:

Nuclear factor of activate T-cells

NGF:

Nerve growth factor

PI3K:

Phosphoinositide 3-kinase

PPAR:

Peroxisome proliferator-activated receptor

ROS:

Reactive oxygen species

RTK:

Receptor tyrosine kinase

shRNA:

Short hairpin RNA

siRNA:

Small interference RNA

TRP:

Transient receptor potential

VEGF:

Vascular endothelial growth factor

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Acknowledgements

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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Authors and Affiliations

  1. Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Madrid, Spain

    Clara Andradas, Eduardo Pérez-Gómez, Manuel Guzmán & Cristina Sánchez

  2. Department of Pathology, University of Cambridge, Cambridge, UK

    María M. Caffarel

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  1. Clara Andradas
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  2. María M. Caffarel
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  3. Eduardo Pérez-Gómez
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  4. Manuel Guzmán
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  5. Cristina Sánchez
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Correspondence to Cristina Sánchez .

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Editors and Affiliations

  1. , Anatomy and Cell Biology, Temple University School of Medicine, 3500 N. Broad Street, Philadelphia, 19140, Pennsylvania, USA

    Mary E. Abood

  2. National Institutes of Health, Division of Basic Neuroscience and Behav, National Institute on Drug Abuse, 6001 Executive Blvd, Bethesda, 20892, Maryland, USA

    Roger G Sorensen

  3. , Pharmacology and Psychiatry and Behavior, University of Washington, Box 357280, Seattle, 98195, Washington, USA

    Nephi Stella

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Andradas, C., Caffarel, M.M., Pérez-Gómez, E., Guzmán, M., Sánchez, C. (2013). The Role of GPR55 in Cancer. In: Abood, M., Sorensen, R., Stella, N. (eds) endoCANNABINOIDS. The Receptors, vol 24. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-4669-9_5

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