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
-
Pioglitazone and Cancer: Angel or Demon?
Current Pharmaceutical Design The Role of Ghrelin Signals in Breast Cancer- A Systematic Review
Current Signal Transduction Therapy A Comparison Between Bisphosphonates and Other Treatments for Osteoporosis
Current Pharmaceutical Design Melanocortins in the Treatment of Male and Female Sexual Dysfunction
Current Topics in Medicinal Chemistry Pharmacogenetics and Statin Treatment: Reality or Theory?
Current Vascular Pharmacology New Development and Application of Ultrasound Targeted Microbubble Destruction in Gene Therapy and Drug Delivery
Current Gene Therapy Editorial: Recent Advances in Drug Delivery Technology
Drug Delivery Letters Graphical Abstracts
Letters in Drug Design & Discovery Impact of PLK-1 Silencing on Endothelial Cells and Cancer Cells of Diverse Histological Origin
Current Gene Therapy Recent Progress in the Development of Anticancer Agents
Current Medicinal Chemistry - Anti-Cancer Agents Plant Natural Products in Anticancer Drug Discovery
Current Organic Chemistry Somatostatin, Somatostatin Analogs and Somatostatin Receptor Dynamics in the Biology of Cancer Progression
Current Molecular Medicine NRF2-Dependent Glutamate-L-Cysteine Ligase Catalytic Subunit Expression Mediates Insulin Protection Against Hyperglycemia-Induced Brain Endothelial Cell Apoptosis
Current Neurovascular Research α-Halogenoacrylic Derivatives of Antitumor Agents
Mini-Reviews in Medicinal Chemistry IO Nation: The Rise of Immuno-Oncology
Current Pharmacogenomics and Personalized Medicine Inhibitors of the Ubiquitin-Proteasome System and the Cell Death Machinery: How Many Pathways are Activated?
Current Molecular Pharmacology The Role of Apoptosis in Tumor Progression and Metastasis
Current Molecular Medicine Editorial [Hot Topic: New Approaches to Treating Cancer: Medicinal Chemistry and Therapeutic Potential (Guest Editor: David J. Weber)]
Current Topics in Medicinal Chemistry Endogenous Retroelements in Cellular Senescence and Related Pathogenic Processes: Promising Drug Targets in Age-Related Diseases
Current Drug Targets Design of Combretastatin A-4 Analogs as Tubulin Targeted Vascular Disrupting Agent with Special Emphasis on Their Cis-Restricted Isomers
Current Pharmaceutical Design