GPCR and cancer

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Background

G-protein-coupled receptors (GPCRs) are among the largest and most diverse family of proteins in the mammalian genome, which transduce signals as a response to a wide range of stimuli. GPCRs are major targets in drug discovery, as reflected by the fact that they encompass about 50% of current medicinal compounds. In humans, the completed human genome project has led to the identification of over 865 GPCR genes. The diversity of GPCRs is dictated not only by the variety of stimuli that they respond to, but also their participation in various signaling pathways. Their widespread expression, especially on the cell surface, that makes them accessible to antagonists, agonists, hormones and drugs, as well as tissue and cell type specificity, which provide selectivity for the receptors and ligands. Exploration of various drug targets has lead to the identification of multiple ways in which GPCRs contribute to a disease state. Classification of GPCR related diseases fall into categories of either rare
monogenic disease resulting from loss or gain of function mutations in GPCRs, from genetic variants of GPCRs or from defects in G proteins. An example of genetic variants in GPCRs is vitiligo, a disease characterized by the loss of melanocytes resulting in cutaneous white macules, results from studies found more polymorphisms than those with no vitiligo in the GPCR melanocortin 1 receptor (MC1R), which controls melanomagenesis. The polymorphisms in GPCRs can also have a protective effect against infections as observed in HIV. In studies examining HIV infection resistance in people with multiple exposures to the virus, led to the identification of homozygous loss-of-function mutations of the type 5 chemokine receptor (CCR5) that confer resistance to HIV infection as CCR5 serves as a co-receptor for HIV entry into the target cell. Defects in G proteins especially Gα subunits (transducin and Gsα) are also associated with human diseases. Mutations in transducin cause it to uncouple from its effector and has been associated with the Nougaret form of autosomal dominant stationary night blindness. Mutations in Gβ or Gγ have not been associated with any monogenic human disorders to-date, but a polymorphism of the β3 subunit has been implicated in several common multigenic disorders. GPCRs have been known to have oncogenic properties since the identification of a potential oncogene, Mas. Mas, was found to be capable of transforming murine NIH 3T3 fibroblasts with weak foci forming ability in vitro but were tumorigenic in nude mice in vivo. Unlike the oncogenes discovered earlier activating mutations were not established in Mas. Subsequent studies revealed that a normal GPCR could possess oncogenic characteristic as a result of its ectopic expression or the formation of autocrine/paracrine loops. There is now compelling evidence that some members of GPCR family could induce oncogenic transformation by alteration of GPCR expression level. Much remains to know the underlying mechanisms on GPCRs and human cancer.

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