), an organ-specific chemokine receptor, interacts with its exclusive ligand CCL25 to promote tumor proliferation In vitro , SACC cell proliferation and apoptosis were evaluated using Cell Counting Kit-8 and colon formation

They have participated in various cellular processes such as cell proliferation, migration, apoptosis

protein-coupled receptor kinase 2 is essential to enable vasoconstrictor-mediated arterial smooth muscle proliferation arterial contraction and stimulates signalling pathways that promote vascular smooth muscle cell (VSMC) proliferation GPCR signalling through phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) promotes VSMC proliferation implicated in controlling various aspects of cellular growth, we examined whether GRK2 could affect VSMC proliferation These data suggest GRK2 expression is essential to facilitate vasoconstrictor-driven VSMC proliferation

Oncology and Immunology Vasoactive intestinal peptide receptor 2 signaling promotes breast cancer cell proliferation However, the pathophysiological role of increased VIPR2 in the proliferation of breast cancer cells remains that VIPR2 overexpression in MCF-7 and MDA-MB-231 cells, human breast cancer cell lines, promoted cell proliferation Increased VIPR2 also exacerbated intraperitoneal proliferation of breast cancer MDA-MB-231 cells in a Moreover, an inhibitor of mitogen-activated protein kinase kinase, U0126, attenuated tumor proliferation

< GPCR News < GPCRs in Oncology and Immunology RGS20 promotes non-small cell lung carcinoma proliferation CCK8 and cell cloning were conducted to determine the proliferation ability of H1299 and Anip973 cells In vitro and in vivo experiments verified whether overexpression of RGS20 affect the proliferation and Further, RGS20 accelerated cell proliferation by increasing autophagy. Conclusion: Our findings indicate that RGS20 drives NSCLC cell proliferation by triggering autophagy

Pharmacological inhibition of neuropeptide Y receptors Y1 and Y5 reduces hypoxic breast cancer migration, proliferation inducible factors, which sensitizes these receptors to NPY stimulation leading to enhanced migration and proliferation Here, we measured the effects of NPY1R and NPY5R antagonists in normoxia and hypoxia on migration, proliferation Antagonizing NPY1R and/or NPY5R in hypoxia compared to normoxia more greatly reduced MAPK signaling, cell proliferation