Formyl peptide receptors at the interface of inflammation, angiogenesis and tumor growth

被引:89
作者
Prevete, Nella [1 ]
Liotti, Federica [2 ,3 ]
Marone, Gianni [1 ,3 ,4 ]
Melillo, Rosa Marina [2 ,3 ]
de Paulis, Amato [1 ,4 ]
机构
[1] Univ Naples Federico II, Dept Translat Med Sci DiSMeT, I-80131 Naples, Italy
[2] Univ Naples Federico II, Dept Mol Med & Med Biotechnol, I-80131 Naples, Italy
[3] CNR, Inst Endocrinol & Expt Oncol IEOS G Salvatore, I-80131 Naples, Italy
[4] Univ Naples Federico II, Ctr Basic & Clin Immunol Res CISI, I-80731 Naples, Italy
关键词
PRORESOLVING LIPID MEDIATORS; SIGNAL-TRANSDUCTION; EPITHELIAL-CELLS; FORMYLPEPTIDE RECEPTOR; LEUKOCYTE RECRUITMENT; APOPTOTIC CELLS; VEGF EXPRESSION; CYCLOSPORINE-H; RESOLUTION; ACTIVATION;
D O I
10.1016/j.phrs.2015.09.017
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
N-formyl peptide receptors (FPRs) belong to the family of pattern recognition receptors (PRRs) that regulate innate immune responses. Three FPRs have been identified in humans: FPR1-FPR3. FPR expression was initially described in immune cells and subsequently in non-hematopoietic cells and certain tissues. Besides their involvement in inflammatory disorders, FPRs have been implicated in the regulation of tissue repair and angiogenesis.Angiogenesis is not only a key component of pathogen defence during acute infection and of chronic inflammatory disorders, but also plays a critical role in wound healing and tissue regeneration. Moreover, pathologic uncontrolled angiogenesis is central for tumour growth, progression, and the formation of metastases. In this review, we summarise the evidence for a central role of FPRs at the intersection between inflammation, physiologic angiogenesis and pathologic neovascularisation linked to cancer. These findings provide insights into the potential clinical relevance of new treatment regimens involving FPR modulation. (C) 2015 Elsevier Ltd. All rights reserved.
引用
收藏
页码:184 / 191
页数:8
相关论文
共 74 条
[1]   Redox signaling regulates commensal-mediated mucosal homeostasis and restitution and requires formyl peptide receptor 1 [J].
Alam, A. ;
Leoni, G. ;
Wentworth, C. C. ;
Kwal, J. M. ;
Wu, H. ;
Ardita, C. S. ;
Swanson, P. A. ;
Lambeth, J. D. ;
Jones, R. M. ;
Nusrat, A. ;
Neish, A. S. .
MUCOSAL IMMUNOLOGY, 2014, 7 (03) :645-655
[2]   Formyl peptide receptor-1 activation enhances intestinal epithelial cell restitution through phosphatidylinositol 3-kinase-dependent activation of Rac1 and Cdc42 [J].
Babbin, Brian A. ;
Jesaitis, Algirdas J. ;
Ivanov, Andrei I. ;
Kelly, Daina ;
Laukoetter, Mike ;
Nava, Porfirio ;
Parkos, Charles A. ;
Nusrat, Asma .
JOURNAL OF IMMUNOLOGY, 2007, 179 (12) :8112-8121
[3]   Inflammation and cancer: back to Virchow? [J].
Balkwill, F ;
Mantovani, A .
LANCET, 2001, 357 (9255) :539-545
[4]   Broad immunocytochemical localization of the formylpeptide receptor in human organs, tissues, and cells [J].
Becker, EL ;
Forouhar, FA ;
Grunnet, ML ;
Boulay, F ;
Tardif, M ;
Bormann, BJ ;
Sodja, D ;
Ye, RD ;
Woska, JR ;
Murphy, PM .
CELL AND TISSUE RESEARCH, 1998, 292 (01) :129-135
[5]  
BIFULCO K, 2010, THROMB HAEMOSTASIS, V8, P2789, DOI DOI 10.1111/J.1538-7836.2010.04075.X
[6]   uPAR-uPA-PAI-l interactions and signaling: A vascular biologist's view [J].
Binder, Bernd R. ;
Mihaly, Judit ;
Prager, Gerald W. .
THROMBOSIS AND HAEMOSTASIS, 2007, 97 (03) :336-342
[7]   uPAR: A versatile signalling orchestrator [J].
Blasi, F ;
Carmeliet, P .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2002, 3 (12) :932-943
[8]   Inhibition of formyl peptide receptor in high-grade astrocytoma by CHemotaxis Inhibitory Protein of S. aureus [J].
Boer, J. C. ;
Domanska, U. M. ;
Timmer-Bosscha, H. ;
Boer, I. G. J. ;
de Haas, C. J. C. ;
Joseph, J. V. ;
Kruyt, F. A. E. ;
de Vries, E. G. E. ;
den Dunnen, W. F. A. ;
van Strijp, J. A. G. ;
Walenkamp, A. M. E. .
BRITISH JOURNAL OF CANCER, 2013, 108 (03) :587-596
[9]   INHIBITION OF RECEPTOR-MEDIATED RELEASE OF ARACHIDONIC-ACID BY PERTUSSIS TOXIN [J].
BOKOCH, GM ;
GILMAN, AG .
CELL, 1984, 39 (02) :301-308
[10]  
BOKOCH GM, 1984, J BIOL CHEM, V259, P3560