Abstract
The receptor for the lipid mediator PAF (PAFR) is a G-protein coupled receptor expressed in several cell types. Besides PAF, a series of oxidized phospholipids can also bind to PAFR. Dying cells also express PAFR-ligands and, in both situations, scavenger receptors are involved as well. There is evidence that the scavenger receptor CD36 and PAFR associate in the macrophages membrane and signal in conjunction to induce a regulatory phenotype. In the tumor microenvironment, apoptotic cells are abundant due to hypoxia, and PAF-like phospholipids are generated. Engagement of PAFR expressed by tumor macrophages and dendritic cells induces a regulatory/tolerogenic phenotype and subverts the innate and adaptive immune response to the tumor. During cancer therapies, PAFR-ligands can be generated, further aggravating the immune suppression. Moreover, some tumor cells express PAFR and its activation by PAFR-ligands generated during chemotherapy induce anti-apoptotic factors, which protect the tumor cells from death induced by these treatments. It is proposed that PAFR antagonists, administered in combination with chemotherapy, may represent a promising strategy for cancer treatment.
Keywords: Chemotherapy, PAF receptor, tumor growth, tumor macrophages, tumor microenvironment.
Current Drug Targets
Title:PAF Receptor and Tumor Growth
Volume: 15 Issue: 10
Author(s): Sonia Jancar and Roger Chammas
Affiliation:
Keywords: Chemotherapy, PAF receptor, tumor growth, tumor macrophages, tumor microenvironment.
Abstract: The receptor for the lipid mediator PAF (PAFR) is a G-protein coupled receptor expressed in several cell types. Besides PAF, a series of oxidized phospholipids can also bind to PAFR. Dying cells also express PAFR-ligands and, in both situations, scavenger receptors are involved as well. There is evidence that the scavenger receptor CD36 and PAFR associate in the macrophages membrane and signal in conjunction to induce a regulatory phenotype. In the tumor microenvironment, apoptotic cells are abundant due to hypoxia, and PAF-like phospholipids are generated. Engagement of PAFR expressed by tumor macrophages and dendritic cells induces a regulatory/tolerogenic phenotype and subverts the innate and adaptive immune response to the tumor. During cancer therapies, PAFR-ligands can be generated, further aggravating the immune suppression. Moreover, some tumor cells express PAFR and its activation by PAFR-ligands generated during chemotherapy induce anti-apoptotic factors, which protect the tumor cells from death induced by these treatments. It is proposed that PAFR antagonists, administered in combination with chemotherapy, may represent a promising strategy for cancer treatment.
Export Options
About this article
Cite this article as:
Jancar Sonia and Chammas Roger, PAF Receptor and Tumor Growth, Current Drug Targets 2014; 15 (10) . https://dx.doi.org/10.2174/1389450115666140903111812
DOI https://dx.doi.org/10.2174/1389450115666140903111812 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
Call for Papers in Thematic Issues
New drug therapy for eye diseases
Eyesight is one of the most critical senses, accounting for over 80% of our perceptions. Our quality of life might be significantly affected by eye disease, including glaucoma, diabetic retinopathy, dry eye, etc. Although the development of microinvasive ocular surgery reduces surgical complications and improves overall outcomes, medication therapy is ...read more
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Contrast-enhanced Ultrasound for Liver Imaging: Recent Advances
Current Pharmaceutical Design Novel Rational Drug Design Strategies with Potential to Revolutionize Malaria Chemotherapy
Current Medicinal Chemistry Matrix Metalloproteinases
Current Medicinal Chemistry Molecular Sieves in Medicine
Mini-Reviews in Medicinal Chemistry Th17 and Treg Cells, Two New Lymphocyte Subpopulations with a Key Role in the Immune Response Against Infection
Infectious Disorders - Drug Targets Imaging of Integrins as Biomarkers for Tumor Angiogenesis
Current Pharmaceutical Design Functionalized Carbon Nano-scale Drug Delivery Systems From Biowaste Sago Bark For Cancer Cell Imaging
Current Drug Delivery Regulation of the Endoplasmic Reticulum Ca2+-Store in Cancer
Anti-Cancer Agents in Medicinal Chemistry Cell Responses to Oxidative Stressors
Current Pharmaceutical Design Recombinant Salmonella Vaccination Technology and Its Application to Human Bacterial Pathogens
Current Pharmaceutical Biotechnology Network of WNT and Other Regulatory Signaling Cascades in Pluripotent Stem Cells and Cancer Stem Cells
Current Pharmaceutical Biotechnology The Exploitation of Toll-like Receptor 3 Signaling in Cancer Therapy
Current Pharmaceutical Design Combinatorial Nanoparticles for Cancer Diagnosis and Therapy
Current Medicinal Chemistry New Insights Into Biology of Chronic Myeloid Leukemia: Implications in Therapy
Current Cancer Drug Targets Acrylamide Induced Toxicity and the Propensity of Phytochemicals in Amelioration: A Review
Central Nervous System Agents in Medicinal Chemistry Oxazol-5-(4H)-Ones. Part 1. Synthesis and Reactivity as 1,3-dipoles
Current Organic Chemistry Caring for HIV-Infected Patients in the ICU in The Highly Active Antiretroviral Therapy Era
Current HIV Research A Curcumin Analog, GO-Y078, Effectively Inhibits Angiogenesis through Actin Disorganization
Anti-Cancer Agents in Medicinal Chemistry Preparation and Characterization of Methylene blue Nanoparticles for Alzheimer's Disease and Other Tauopathies
Current Drug Delivery Cytochromes P450 in Brain: Function and Significance
Current Drug Metabolism