Special Issue "G-Protein Coupled Receptors in Cancer"
Deadline for manuscript submissions: closed (15 January 2022) | Viewed by 29808
G-protein-coupled receptors (GPCRs) are the largest family of plasma membrane receptors. Signaling by heterotrimeric G-proteins begins when ligand binding to the GPCR triggers a conformational change promoting proximity of the GEF domain and the GDP-bound heterotrimeric G-protein. GTP exchange liberates the a-subunit from the bg-subunits and initiates signal transduction. G-protein inactivation occurs when GTP hydrolyses to GDP in the a-subunit (promoted by RGS proteins) and the bg-subunits re-associate. The pathway may also be inhibited by phosphorylation of the GPCR by protein kinases, the subsequent binding of arrestin proteins, and internalization of the receptor through clathrin-coated pits. Despite mediating a cornucopia of physiological processes, the role of GPCRs in tumor biology is underappreciated. GPCRs, their ligands, and downstream effectors significantly regulate tumor growth and metastasis but influence tumor and stromal cells alike. The normal physiological functions of GPCRs are often hijacked by malignant cells to promote cell survival and proliferation, immune cell evasion, local and distant invasion, and recruitment of blood vessels.
This Special Issue of Cells invites both original research and review articles that examine the role of GPCRs, their G-protein targets and their regulatory apparatus (RGSs, GRKs) in tumorigenesis (including the role of point mutations, gene overexpression, and epigenetic promoter silencing), and stromal and immune responses in the tumor milieu. We will also discuss the unique opportunities for targeting GPCRs for therapeutic gain in cancers without current therapy and those refractory to current approaches.
Dr. Anthony Ashton
Manuscript Submission Information
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