The relevance of the chemokine receptor ACKR3/CXCR7 on CXCL12-mediated effects in cancers with a focus on virus-related cancers |
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| Institution: | 2. Department of Medical Oncology, Sidney Kimmel Cancer Center, Thomas Jefferson University, 233 S. 10th Street, Philadelphia, PA 19107;3. Department of Pathology and Laboratory Medicine, Drexel University College of Medicine, 245 N. 15th Street, Philadelphia, PA 19012;4. Biology of Prostate Cancer Program, Sidney Kimmel Cancer Center, Thomas Jefferson University, 233 S. 10th Street, Philadelphia, PA 19107;5. Department of Microbiology and Immunology, Drexel University College of Medicine, 245 N. 15th Street, Philadelphia, PA 19102;1. Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden;2. Department of Infection and Immunity, Immuno-Pharmacology and Interactomics, Luxembourg Institute of Health (LIH), Esch-sur-Alzette, Luxembourg;3. amcure GmbH, Eggenstein-Leopoldshafen, Germany |
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| Abstract: | Recent studies have highlighted the importance of understanding the molecular determinants of CXCL12-mediated effects in cancers. Once previously thought to interact exclusively with CXCR4, CXCL12 also binds with high affinity to CXCR7 (recently renamed ACKR3), which belongs to an atypical chemokine receptor family whose members fail to activate Gαi proteins but interact with β-arrestins. In addition to its capacity to control CXCL12 bioavailability, ACKR3 can either enhance or dampen CXCR4-mediated signaling and activity. In light of the most recent findings, we have examined the role of ACKR3 in cancer, including a subset of virus-related cancers. |
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| Keywords: | Cancer Virus ACKR3/CXCR7 CXCL12/SDF-1 CXCR4 |
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