Formyl peptide receptor 1 suppresses gastric cancer angiogenesis and growth by exploiting inflammation resolution pathways
| Autor: | Piero Pucci, Angela Amoresano, Anna Illiano, Nella Prevete, Federica Liotti, Rosa Marina Melillo, Amato de Paulis |
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| Přispěvatelé: | Prevete, Nella, Liotti, Federica, Illiano, Anna, Amoresano, Angela, Pucci, Pietro, DE PAULIS, Amato, Melillo, ROSA MARINA |
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
lcsh:Immunologic diseases. Allergy Angiogenesis Immunology pro-resolving pathways Inflammation Endogeny Biology lcsh:RC254-282 Formyl peptide receptor 1 formyl peptide receptors 03 medical and health sciences angiogenesis 0302 clinical medicine medicine Immunology and Allergy resolvin d1 Receptor Original Research formyl peptide receptor gastric cancer lipoxin b4 Cancer medicine.disease lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ALOX15 GPR32 Angiogenesi pro-resolving pathway 030104 developmental biology Oncology Biochemistry 030220 oncology & carcinogenesis Cancer research medicine.symptom lcsh:RC581-607 |
| Zdroj: | OncoImmunology, Vol 6, Iss 4 (2017) ONCOIMMUNOLOGY 6 (2017). doi:10.1080/2162402X.2017.1293213 info:cnr-pdr/source/autori:Prevete, Nella; Liotti, Federica; Illiano, Anna; Amoresano, Angela; Pucci, Piero; de Paulis, Amato; Melillo, Rosa Marina/titolo:Formyl peptide receptor 1 suppresses gastric cancer angiogenesis and growth by exploiting inflammation resolution pathways/doi:10.1080%2F2162402X.2017.1293213/rivista:ONCOIMMUNOLOGY/anno:2017/pagina_da:/pagina_a:/intervallo_pagine:/volume:6 |
| DOI: | 10.1080/2162402X.2017.1293213 |
| Popis: | Chronic inflammation can result from inadequate engagement of resolution mechanisms, mainly accomplished by specialized pro-resolving mediators (SPMs) arising from the metabolic activity of lipoxygenases (ALOX5/15) on omega-6 or omega-3 essential polyunsaturated fatty acids (PUFA). We previously demonstrated that formyl peptide receptor 1 (FPR1) suppresses gastric cancer (GC) by inhibiting its inflammatory/angiogenic potential. In this study, we asked whether FPR1 exploits inflammation resolution pathways to suppress GC angiogenesis and growth. Here, we demonstrate that genetic or pharmacologic modulation of FPR1 in GC cells regulated ALOX5/15 expression and production of the SPMs Resolvin D1 (RvD1) and Lipoxin B4 (LXB4). SPM treatment of GC cells abated their angiogenic potential. Genetic deletion of ALOX15 or of the RvD1 receptor GPR32 increased the angiogenic and tumorigenic activity of GC cells thereby mimicking FPR1 loss. Deletion/inhibition of ALOX5/15 or GPR32 blocked FPR1-mediated anti-angiogenic activities, indicating that ALOX5/15 and GPR32 are required for FPR1's pro-resolving action. An omega-3- or omega-6-enriched diet enforced SPM endogenous production in mice and inhibited growth of shFPR1 GC xenografts by suppressing their angiogenic activity. These data implicate that FPR1 and/or pro-resolving pathway components might be used as risk/prognostic markers for GC; omega-6/3-enriched diets, and targeting FPR1 or SPM machinery may be exploited for GC management. |
| Databáze: | OpenAIRE |
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