Formyl Peptide Receptor Suppresses Melanoma Development and Promotes NK Cell Migration

详细信息    查看全文

• 作者：Jian Liu (1)
  Jun Li (2)
  Xiang Zeng (3)
  Zhiguo Rao (1)
  Jianfei Gao (1)
  Bicheng Zhang (1)
  Yong Zhao (1)
  Bo Yang (1)
  Zhigang Wang (1)
  Lifang Yu (1)
  Weixing Wang (1)
  
• 关键词：FPR ; NK cell ; ERK ; melanoma
• 刊名：Inflammation
• 出版年：2014
• 出版时间：June 2014
• 年：2014
• 卷：37
• 期：3
• 页码：984-992
• 全文大小：
• 参考文献：1. Wakita, D., K. Sumida, Y. Iwakura, H. Nishikawa, T. Ohkuri, K. Chamoto, et al. 2010. Tumor-infiltrating IL-17-producing gammadelta T cells support the progression of tumor by promoting angiogenesis. / European Journal of Immunology 40: 1927-937. CrossRef
  2. Croci, D.O., M.F. Zacarias Fluck, M.J. Rico, P. Matar, G.A. Rabinovich, and O.G. Scharovsky. 2007. Dynamic cross-talk between tumor and immune cells in orchestrating the immunosuppressive network at the tumor microenvironment. / Cancer Immunology, Immunotherapy : CII 56: 1687-700. CrossRef
  3. Li, L., L.N. Liu, S. Feller, C. Allen, R. Shivakumar, J. Fratantoni, et al. 2010. Expression of chimeric antigen receptors in natural killer cells with a regulatory-compliant non-viral method. / Cancer Gene Therapy 17: 147-54. CrossRef
  4. Le, Y., J.J. Oppenheim, and J.M. Wang. 2001. Pleiotropic roles of formyl peptide receptors. / Cytokine & Growth Factor Reviews 12: 91-05. CrossRef
  5. Le, Y., Y. Yang, Y. Cui, H. Yazawa, W. Gong, C. Qiu, et al. 2002. Receptors for chemotactic formyl peptides as pharmacological targets. / International Immunopharmacology 2: 1-3. CrossRef
  6. Gao, J.L., E.J. Lee, and P.M. Murphy. 1999. Impaired antibacterial host defense in mice lacking the / N-formylpeptide receptor. / The Journal of Experimental Medicine 189: 657-62. CrossRef
  7. Chen, K., Y. Le, Y. Liu, W. Gong, G. Ying, J. Huang, et al. 2010. A critical role for the g protein-coupled receptor mFPR2 in airway inflammation and immune responses. / Journal of Immunology 184: 3331-335. CrossRef
  8. French, A.R., and W.M. Yokoyama. 2003. Natural killer cells and viral infections. / Current Opinion in Immunology 15: 45-1. CrossRef
  9. Wu, J., and L.L. Lanier. 2003. Natural killer cells and cancer. / Advances in Cancer Research 90: 127-56. CrossRef
  10. Robertson, M.J. 2002. Role of chemokines in the biology of natural killer cells. / Journal of Leukocyte Biology 71: 173-83.
  11. Kim, S.D., J.M. Kim, S.H. Jo, H.Y. Lee, S.Y. Lee, J.W. Shim, et al. 2009. Functional expression of formyl peptide receptor family in human NK cells. / Journal of Immunology 183: 5511-517. CrossRef
  12. Liu, Y., K. Chen, C. Wang, W. Gong, T. Yoshimura, M. Liu, et al. 2013. Cell surface receptor FPR2 promotes antitumor host defense by limiting M2 polarization of macrophages. / Cancer Research 73: 550-60. CrossRef
  13. Kim, H.K., H. Zhang, H. Li, T.T. Wu, S. Swisher, D. He, et al. 2008. Slit2 inhibits growth and metastasis of fibrosarcoma and squamous cell carcinoma. / Neoplasia 10: 1411-420. CrossRef
  14. He, D., H. Li, N. Yusuf, C.A. Elmets, J. Li, J.D. Mountz, et al. 2010. IL-17 promotes tumor development through the induction of tumor promoting microenvironments at tumor sites and myeloid-derived suppressor cells. / Journal of Immunology 184: 2281-288. CrossRef
  15. Kim, S.D., S. Kwon, S.K. Lee, M. Kook, H.Y. Lee, K.D. Song, et al. 2013. The immune-stimulating peptide WKYMVm has therapeutic effects against ulcerative colitis. / Experimental & Molecular Medicine 45: e40. CrossRef
  16. Holobotovskyy, V., M. Manzur, M. Tare, J. Burchell, E. Bolitho, H. Viola, et al. 2013. Regulator of G-protein signaling 5 controls blood pressure homeostasis and vessel wall remodeling. / Circulation Research 112: 781-91. CrossRef
  17. Wang, G., M. Tschoi, R. Spolski, Y. Lou, K. Ozaki, C. Feng, et al. 2003. In vivo antitumor activity of interleukin 21 mediated by natural killer cells. / Cancer Research 63: 9016-022.
  18. Gabrilovich, D.I., and S. Nagaraj. 2009. Myeloid-derived suppressor cells as regulators of the immune system. / Nature Reviews Immunology 9: 162-74. CrossRef
  19. Marigo, I., L. Dolcetti, P. Serafini, P. Zanovello, and V. Bronte. 2008. Tumor-induced tolerance and immune suppression by myeloid derived suppressor cells. / Immunological Reviews 222: 162-79. CrossRef
  20. Bronte, V., and P. Zanovello. 2005. Regulation of immune responses by l -arginine metabolism. / Nature Reviews Immunology 5: 641-54. CrossRef
  21. Maghazachi, A.A., A. al-Aoukaty, and T.J. Schall. 1994. C-C chemokines induce the chemotaxis of NK and IL-2-activated NK cells. Role for G proteins. / Journal of Immunology 153: 4969-977.
  22. Sebok, K., D. Woodside, A. al-Aoukaty, A.D. Ho, S. Gluck, and A.A. Maghazachi. 1993. IL-8 induces the locomotion of human IL-2-activated natural killer cells. Involvement of a guanine nucleotide binding (Go) protein. / Journal of immunology 150: 1524-534.
  23. Scharton-Kersten, T., and P. Scott. 1995. The role of the innate immune response in Th1 cell development following / Leishmania major infection. / Journal of Leukocyte Biology 57: 515-22.
  24. Le, Y., W. Gong, B. Li, N.M. Dunlop, W. Shen, S.B. Su, et al. 1999. Utilization of two seven-transmembrane, G protein-coupled receptors, formyl peptide receptor-like 1 and formyl peptide receptor, by the synthetic hexapeptide WKYMVm for human phagocyte activation. / Journal of Immunology 163: 6777-784.
  25. Dahlgren, C., T. Christophe, F. Boulay, P.N. Madianos, M.J. Rabiet, and A. Karlsson. 2000. The synthetic chemoattractant Trp-Lys-Tyr-Met-Val-DMet activates neutrophils preferentially through the lipoxin A(4) receptor. / Blood 95: 1810-818.
  26. Pohajdak, B., J. Gomez, F.W. Orr, N. Khalil, M. Talgoy, and A.H. Greenberg. 1986. Chemotaxis of large granular lymphocytes. / Journal of Immunology 136: 278-84.
  27. Ruth, J.H., C.S. Haas, C.C. Park, M.A. Amin, R.J. Martinez, G.K. Haines 3rd, et al. 2006. CXCL16-mediated cell recruitment to rheumatoid arthritis synovial tissue and murine lymph nodes is dependent upon the MAPK pathway. / Arthritis and Rheumatism 54: 765-78. CrossRef
  28. Serafini, P., I. Borrello, and V. Bronte. 2006. Myeloid suppressor cells in cancer: recruitment, phenotype, properties, and mechanisms of immune suppression. / Seminars in Cancer Biology 16: 53-5. CrossRef
  29. Joyce, J.A., and J.W. Pollard. 2009. Microenvironmental regulation of metastasis. / Nature Reviews Cancer 9: 239-52. CrossRef
  30. Gordon, S., and P.R. Taylor. 2005. Monocyte and macrophage heterogeneity. / Nature Reviews Immunology 5: 953-64. CrossRef
  31. Talmadge, J.E., M. Donkor, and E. Scholar. 2007. Inflammatory cell infiltration of tumors: Jekyll or Hyde. / Cancer Metastasis Reviews 26: 373-00. CrossRef
  32. Mosser, D.M., and J.P. Edwards. 2008. Exploring the full spectrum of macrophage activation. / Nature Reviews Immunology 8: 958-69. CrossRef
  33. Afonina, I.S., S.P. Cullen, and S.J. Martin. 2010. Cytotoxic and non-cytotoxic roles of the CTL/NK protease granzyme B. / Immunological Reviews 235: 105-16.
  34. Schwarz, E.C., B. Qu, and M. Hoth. 1833. Calcium, cancer and killing: the role of calcium in killing cancer cells by cytotoxic T lymphocytes and natural killer cells. / Biochimica et Biophysica acta 2013: 1603-611.
  35. Azogui, O., M.F. Avril, A. Margulis, M. Guillard, B. Caillou, and M. Prade. 1991. Tumor-infiltrating CD3- NK cells are more effective than CD3+ T cells in killing autologous melanoma cells. / The Journal of Investigative Dermatology 97: 425-29. CrossRef
  36. Vesely, M.D., M.H. Kershaw, R.D. Schreiber, and M.J. Smyth. 2011. Natural innate and adaptive immunity to cancer. / Annual Review of Immunology 29: 235-71. CrossRef
  37. Schroder, K., M.J. Sweet, and D.A. Hume. 2006. Signal integration between IFNgamma and TLR signalling pathways in macrophages. / Immunobiology 211: 511-24. CrossRef
  38. Kang, H.K., H.Y. Lee, M.K. Kim, K.S. Park, Y.M. Park, J.Y. Kwak, et al. 2005. The synthetic peptide Trp-Lys-Tyr-Met-Val-D-Met inhibits human monocyte-derived dendritic cell maturation via formyl peptide receptor and formyl peptide receptor-like 2. / Journal of Immunology 175: 685-92. CrossRef
  
• 作者单位：Jian Liu (1)
  Jun Li (2)
  Xiang Zeng (3)
  Zhiguo Rao (1)
  Jianfei Gao (1)
  Bicheng Zhang (1)
  Yong Zhao (1)
  Bo Yang (1)
  Zhigang Wang (1)
  Lifang Yu (1)
  Weixing Wang (1)
  
  1. Department of Oncology, Wuhan General Hospital of Guangzhou Command, People’s Liberation Army, 627 Wuluo Road, Wuhan, 430070, China
  2. Department of Oncology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
  3. Department of Oncology, General Hospital of The Yangtze River Shipping, Wuhan, China
  
• ISSN：1573-2576

文摘

In order to understand how tumor cells can escape immune surveillance mechanisms and thus develop antitumor therapies, it is critically important to investigate the mechanisms by which the immune system interacts with the tumor microenvironment. In our current study, wild-type mice were inoculated with melanoma cell line B16-F10 (1?×-06/mouse) and treated with the formyl peptide receptor (FPR) agonist WKYMVm or the FPR antagonist WRW4. Growth of melanoma cell line B16-F10 was significantly inhibited in WKYMVm-treated mice and markedly promoted in WRW4-treated mice compared with control. Decreased number of myeloid-derived suppressor cells (MDSCs) and increased NK cell infiltration in tumor tissues were detected from WKYMVm-treated mice. Next, we showed that depletion of NK cell significantly increased tumor development in B16 tumor-bearing mice compared with the control group, and the suppressed tumor-developing effect of WKYMVm in B16 melanoma was abrogated with NK cell depletion. We also found that WKYMVm stimulates chemotactic migration in NK cells via the FPR family, and this was dependent on extracellular signal-related kinase (ERK) activation. Moreover, in our further experiment, we showed that the increased infiltration of NK cell and promoted NK cell chemotaxis in B16 melanoma induced by WKYMVm were both abolished with ERK inhibitor PD98059 administration. In conclusion, the FPR family promoted NK cell migration through ERK activation and inhibited B16 melanoma growth in a murine model.