Abstract
G-coupled protein receptors (GCPR) involve several signaling pathways, some of them being coupled with intracellular calcium (Ca2+) mobilization. GPCRs were involved in migration, invasion and metastasis of different types of cancers, including ovarian cancer. Many studies have discussed the essential contribution of GPCRs activated by steroid hormones in ovarian cancer. However, ovarian cancer is also associated with altered signals coming from the nervous system, the immune system or the inflammatory environment, in which GPCRs are ‘sensing’ these molecular signals. Many studies have been oriented so far on ovarian cell lines (most of them being of human cell lines), and only few studies based on animal models or clinical studies have been devoted to the expression changes or functional role of GPCRs in ovarian cancer. In this paper, we review the alterations of GPCRs activated by neurotransmitters (muscarinic receptors, serotonin receptors, dopamine receptors, adrenoceptors) or inflammation-associated molecules (bradykinin receptors, histamine receptors, chemokine receptors) in ovarian cancer and we discuss their potential as histological biomarkers.
Highlights
G-protein-coupled receptors (GPCRs) are seven-transmembrane receptors coupled to heterotrimeric G-proteins encoded by the largest gene family in the human genome
When a ligand binds to the GPCR, guanine diphosphate (GDP) is released and replaced by guanosine triphosphate (GTP), while the subunits are dissociated into a βγ dimer and the GTP bound α monomer (Figure 1)
There is a great body of evidence describing the contribution of G-protein coupled estrogen receptors in ovarian cancer, both in cell lines and in patient studies [14,15,16,17,18,19,20,21,22,23], some of them signaling though calcium mediated signaling pathways, while others through mitogen-activated protein kinase signaling pathways
Summary
G-protein-coupled receptors (GPCRs) are seven-transmembrane receptors coupled to heterotrimeric G-proteins encoded by the largest gene family in the human genome. The alteration of the signaling cascades activated by GPCRs may trigger gene expression changes and contribute to cell proliferation, angiogenesis, tumor growth, and metastasis in multiple cancers, including ovarian cancer. There is a great body of evidence describing the contribution of G-protein coupled estrogen receptors in ovarian cancer, both in cell lines and in patient studies [14,15,16,17,18,19,20,21,22,23], some of them signaling though calcium mediated signaling pathways, while others through mitogen-activated protein kinase signaling pathways. It is very important to highlight that the mechanisms involved in ovarian cancer staging are more complex than the endocrine alterations In this context, a systematic review dedicated to the contribution of other GPCRs (i.e activated by neurotransmitters or inflammation-related molecules) in ovarian cancer is largely missing. Attention on GPCR-mediated Ca2+ signaling, but in some cases, when relevant for the ovarian cancer pathology, we are discussing the GPCR signaling mediated by other secondary messengers
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