Student or educator? Sign up with your school email and get 6 months of Pro free.
Cited by 2,792

The DOI matches its Crossref record; 119 of the 119 references it cites were found in a registry or an index.

Inflammation and tumor progression: signaling pathways and targeted intervention

Open access
Zhao, Huakan, Wu, Lei, Yan, Guifang, Chen, Yu, Zhou, Mingyue, Wu, Yongzhong, Li, Yongsheng·2021·Signal Transduction and Targeted Therapy

Abstract

Cancer development and its response to therapy are regulated by inflammation, which either promotes or suppresses tumor progression, potentially displaying opposing effects on therapeutic outcomes. Chronic inflammation facilitates tumor progression and treatment resistance, whereas induction of acute inflammatory reactions often stimulates the maturation of dendritic cells (DCs) and antigen presentation, leading to anti-tumor immune responses. In addition, multiple signaling pathways, such as nuclear factor kappa B (NF-kB), Janus kinase/signal transducers and activators of transcription (JAK-STAT), toll-like receptor (TLR) pathways, cGAS/STING, and mitogen-activated protein kinase (MAPK); inflammatory factors, including cytokines (e.g., interleukin (IL), interferon (IFN), and tumor necrosis factor (TNF)-α), chemokines (e.g., C-C motif chemokine ligands (CCLs) and C-X-C motif chemokine ligands (CXCLs)), growth factors (e.g., vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-β), and inflammasome; as well as inflammatory metabolites including prostaglandins, leukotrienes, thromboxane, and specialized proresolving mediators (SPM), have been identified as pivotal regulators of the initiation and resolution of inflammation. Nowadays, local irradiation, recombinant cytokines, neutralizing antibodies, small-molecule inhibitors, DC vaccines, oncolytic viruses, TLR agonists, and SPM have been developed to specifically modulate inflammation in cancer therapy, with some of these factors already undergoing clinical trials. Herein, we discuss the initiation and resolution of inflammation, the crosstalk between tumor development and inflammatory processes. We also highlight potential targets for harnessing inflammation in the treatment of cancer.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/s41392-021-00658-5

Cites

119 of 119 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 119 references

Research works printed but not linked: 787

  1. Tang, W. et al. The mechanisms of sorafenib resistance in hepatocellular carcinoma: theoretical basis and therapeutic aspects. Signal Transduct. Target Ther. 5, 87 (2020). · DOI · Paper page
  2. Grivennikov, S. I., Greten, F. R. & Karin, M. Immunity, inflammation, and cancer. Cell 140, 883–899 (2010). · DOI · Paper page
  3. Crusz, S. M. & Balkwill, F. R. Inflammation and cancer: advances and new agents. Nat. Rev. Clin. Oncol. 12, 584–596 (2015). · DOI · Paper page
  4. Shacter, E. & Weitzman, S. A. Chronic inflammation and cancer. Oncology 16, 217–226 (2002). 229; discussion 230-212.
  5. Schaue, D. et al. Radiation and inflammation. Semin Radiat. Oncol. 25, 4–10 (2015). · DOI · Paper page
  6. Guthrie, G. J. et al. The systemic inflammation-based neutrophil-lymphocyte ratio: experience in patients with cancer. Crit. Rev. Oncol. Hematol. 88, 218–230 (2013). · DOI · Paper page
  7. Balkwill, F. & Mantovani, A. Inflammation and cancer: back to Virchow? Lancet 357, 539–545 (2001). · DOI · Paper page
  8. Punt, S. et al. A beneficial tumor microenvironment in oropharyngeal squamous cell carcinoma is characterized by a high T cell and low IL-17(+) cell frequency. Cancer Immunol. Immunother. 65, 393–403 (2016). · DOI
  9. Elinav, E. et al. Inflammation-induced cancer: crosstalk between tumours, immune cells and microorganisms. Nat. Rev. Cancer 13, 759–771 (2013). · DOI · Paper page
  10. Ma, Y. et al. Anticancer chemotherapy-induced intratumoral recruitment and differentiation of antigen-presenting cells. Immunity 38, 729–741 (2013). · DOI · Paper page
  11. Nathan, C. & Ding, A. Nonresolving inflammation. Cell 140, 871–882 (2010). · DOI · Paper page
  12. Ritter, B. & Greten, F. R. Modulating inflammation for cancer therapy. J. Exp. Med. 216, 1234–1243 (2019). · DOI · Paper page
  13. Cuzick, J. et al. Aspirin and non-steroidal anti-inflammatory drugs for cancer prevention: an international consensus statement. Lancet Oncol. 10, 501–507 (2009). · DOI · Paper page
  14. Rothwell, P. M. et al. Effect of daily aspirin on long-term risk of death due to cancer: analysis of individual patient data from randomised trials. Lancet 377, 31–41 (2011). · DOI · Paper page
  15. Cuzick, J. et al. Estimates of benefits and harms of prophylactic use of aspirin in the general population. Ann. Oncol. 26, 47–57 (2015). · DOI · Paper page
  16. Bonovas, S., Filioussi, K., Tsavaris, N. & Sitaras, N. M. Use of statins and breast cancer: a meta-analysis of seven randomized clinical trials and nine observational studies. J. Clin. Oncol. 23, 8606–8612 (2005). · DOI · Paper page
  17. Maisonneuve, P. & Lowenfels, A. B. Statins and the risk of colorectal cancer. N. Engl. J. Med. 353, 952–954 (2005). author reply 952-954. · DOI
  18. Bonovas, S., Nikolopoulos, G. & Sitaras, N. M. Statins and reduced risk of hepatocellular carcinoma in patients with hepatitis C virus infection: further evidence is warranted. J. Clin. Oncol. 31, 4160 (2013). · doi:10.1200/jco.2013.50.9208
  19. Hao, H. et al. Lipoxin A4 and its analog suppress hepatocellular carcinoma via remodeling tumor microenvironment. Cancer Lett. 309, 85–94 (2011). · DOI
  20. Li, Y. et al. Pleiotropic regulation of macrophage polarization and tumorigenesis by formyl peptide receptor-2. Oncogene 30, 3887–3899 (2011). · DOI · Paper page
  21. Wang, Z. et al. Lipid mediator lipoxin A4 inhibits tumor growth by targeting IL-10-producing regulatory B (Breg) cells. Cancer Lett. 364, 118–124 (2015). · DOI
  22. Mulder, W. J. M. & Gnjatic, S. Cancer immunotherapy: from local to global. Nat. Nanotechnol. 12, 840–841 (2017). · DOI
  23. Gun, S. Y., Lee, S. W. L., Sieow, J. L. & Wong, S. C. Targeting immune cells for cancer therapy. Redox Biol. 25, 101174 (2019). · DOI · Paper page
  24. Davila, M. L. et al. Efficacy and toxicity management of 19-28z CAR T cell therapy in B cell acute lymphoblastic leukemia. Sci. Transl. Med. 6, 224ra225 (2014). · DOI · Paper page
  25. Bonifant, C. L., Jackson, H. J., Brentjens, R. J. & Curran, K. J. Toxicity and management in CAR T-cell therapy. Mol. Ther. Oncolytics 3, 16011 (2016). · DOI · Paper page
  26. Dorward, D. A., Lucas, C. D., Rossi, A. G., Haslett, C. & Dhaliwal, K. Imaging inflammation: molecular strategies to visualize key components of the inflammatory cascade, from initiation to resolution. Pharm. Ther. 135, 182–199 (2012). · DOI
  27. Sun, S. C. The non-canonical NF-kappaB pathway in immunity and inflammation. Nat. Rev. Immunol. 17, 545–558 (2017). · DOI · Paper page
  28. Kono, H. & Rock, K. L. How dying cells alert the immune system to danger. Nat. Rev. Immunol. 8, 279–289 (2008). · DOI · Paper page
  29. Headland, S. E. & Norling, L. V. The resolution of inflammation: Principles and challenges. Semin. Immunol. 27, 149–160 (2015). · DOI · Paper page
  30. Wright, H. L., Moots, R. J., Bucknall, R. C. & Edwards, S. W. Neutrophil function in inflammation and inflammatory diseases. Rheumatology 49, 1618–1631 (2010). · DOI · Paper page
  31. Rossi, A. G. et al. Cyclin-dependent kinase inhibitors enhance the resolution of inflammation by promoting inflammatory cell apoptosis. Nat. Med. 12, 1056–1064 (2006). · DOI · Paper page
  32. Gilroy, D. W., Lawrence, T., Perretti, M. & Rossi, A. G. Inflammatory resolution: new opportunities for drug discovery. Nat. Rev. Drug Disco. 3, 401–416 (2004). · DOI · Paper page
  33. Serhan, C. N. The resolution of inflammation: the devil in the flask and in the details. Faseb J. 25, 1441–1448 (2011). · DOI · Paper page
  34. Kumar, R., Clermont, G., Vodovotz, Y. & Chow, C. C. The dynamics of acute inflammation. J. Theor. Biol. 230, 145–155 (2004). · DOI · Paper page
  35. Serhan, C. N. Controlling the resolution of acute inflammation: a new genus of dual anti-inflammatory and proresolving mediators. J. Periodontol. 79, 1520–1526 (2008). · DOI
  36. Ploeger, H. E., Takken, T., de Greef, M. H. & Timmons, B. W. The effects of acute and chronic exercise on inflammatory markers in children and adults with a chronic inflammatory disease: a systematic review. Exerc. Immunol. Rev. 15, 6–41 (2009).
  37. Boyle, M. et al. Chronic inflammation and angiogenic signaling axis impairs differentiation of dental-pulp stem cells. PLoS ONE 9, e113419 (2014). · DOI
  38. Nasef, N. A., Mehta, S. & Ferguson, L. R. Susceptibility to chronic inflammation: an update. Arch. Toxicol. 91, 1131–1141 (2017). · DOI
  39. Snell, L. M., McGaha, T. L. & Brooks, D. G. Type I interferon in chronic virus infection and cancer. Trends Immunol. 38, 542–557 (2017). · DOI · Paper page
  40. Pollard, K. M. Silica, silicosis, and autoimmunity. Front Immunol. 7, 97 (2016). · DOI · Paper page
  41. Rogovskii, V. Modulation of inflammation-induced tolerance in cancer. Front. Immunol. 11, 1180 (2020). · DOI
  42. DiNicolantonio, J. J. & O’Keefe, J. The importance of maintaining a low omega-6/omega-3 ratio for reducing the risk of inflammatory cytokine storms. Mo. Med. 117, 539–542 (2020).
  43. Kozhieva, M. K. et al. Gut human microbiota and multiple sclerosis. Zh. Nevrol. Psikhiatr Im. S S Korsakova 117, 11–19 (2017). · DOI
  44. Bozkurt, B., Mann, D. L. & Deswal, A. Biomarkers of inflammation in heart failure. Heart Fail Rev. 15, 331–341 (2010). · DOI · Paper page
  45. Glass, C. K., Saijo, K., Winner, B., Marchetto, M. C. & Gage, F. H. Mechanisms underlying inflammation in neurodegeneration. Cell 140, 918–934 (2010). · DOI · Paper page
  46. Kawanishi, S., Ohnishi, S., Ma, N., Hiraku, Y. & Murata, M. Crosstalk between DNA damage and inflammation in the multiple steps of carcinogenesis. Int. J. Mol. Sci 18, 1808 (2017). · DOI · Paper page
  47. Eiro, N. & Vizoso, F. J. Inflammation and cancer. World J. Gastrointest. Surg. 4, 62–72 (2012). · DOI · Paper page
  48. Rogovskii, V. S. The linkage between inflammation and immune tolerance: interfering with inflammation in cancer. Curr. Cancer Drug Targets 17, 325–332 (2017). · doi:10.2174/1568009617666170109110816
  49. Parkin, D. M., Hammerl, L., Ferlay, J. & Kantelhardt, E. J. Cancer in Africa 2018: the role of infections. Int. J. Cancer 146, 2089–2103 (2020). · DOI · Paper page
  50. Hashimoto, M. et al. CD8 T cell exhaustion in chronic infection and cancer: opportunities for interventions. Annu. Rev. Med 69, 301–318 (2018). · DOI · Paper page
  51. Pober, J. S. & Cotran, R. S. The role of endothelial cells in inflammation. Transplantation 50, 537–544 (1990). · DOI · Paper page
  52. Steinke, J. W. & Borish, L. 3. Cytokines and chemokines. J. Allergy Clin. Immunol. 117, S441–S445 (2006). · DOI
  53. Butcher, E. C. Leukocyte-endothelial cell recognition: three (or more) steps to specificity and diversity. Cell 67, 1033–1036 (1991). · DOI · Paper page
  54. Locati, M. & Murphy, P. M. Chemokines and chemokine receptors: biology and clinical relevance in inflammation and AIDS. Annu Rev. Med 50, 425–440 (1999). · DOI · Paper page
  55. Kobayashi, Y. Neutrophil infiltration and chemokines. Crit. Rev. Immunol. 26, 307–316 (2006). · DOI · Paper page
  56. Williams, M. R., Azcutia, V., Newton, G., Alcaide, P. & Luscinskas, F. W. Emerging mechanisms of neutrophil recruitment across endothelium. Trends Immunol. 32, 461–469 (2011). · DOI · Paper page
  57. Simpson, P. J. et al. Reduction of experimental canine myocardial reperfusion injury by a monoclonal antibody (anti-Mo1, anti-CD11b) that inhibits leukocyte adhesion. J. Clin. Invest. 81, 624–629 (1988). · DOI · Paper page
  58. Woodfin, A. et al. The junctional adhesion molecule JAM-C regulates polarized transendothelial migration of neutrophils in vivo. Nat. Immunol. 12, 761–769 (2011). · DOI · Paper page
  59. Corada, M. et al. Junctional adhesion molecule-A-deficient polymorphonuclear cells show reduced diapedesis in peritonitis and heart ischemia-reperfusion injury. Proc. Natl Acad. Sci. USA 102, 10634–10639 (2005). · DOI
  60. Wang, J. Neutrophils in tissue injury and repair. Cell Tissue Res. 371, 531–539 (2018). · DOI · Paper page
  61. Harty, M. W. et al. Neutrophil depletion blocks early collagen degradation in repairing cholestatic rat livers. Am. J. Pathol. 176, 1271–1281 (2010). · DOI
  62. Kuhl, A. A. et al. Aggravation of different types of experimental colitis by depletion or adhesion blockade of neutrophils. Gastroenterology 133, 1882–1892 (2007). · DOI · Paper page
  63. Dewald, O. et al. CCL2/monocyte chemoattractant protein-1 regulates inflammatory responses critical to healing myocardial infarcts. Circ. Res. 96, 881–889 (2005). · DOI · Paper page
  64. Frantz, S. et al. Monocytes/macrophages prevent healing defects and left ventricular thrombus formation after myocardial infarction. FASEB J. 27, 871–881 (2013). · DOI
  65. Zhao, Y., Zou, W., Du, J. & Zhao, Y. The origins and homeostasis of monocytes and tissue-resident macrophages in physiological situation. J. Cell Physiol. 233, 6425–6439 (2018). · DOI
  66. Bystrom, J. et al. Resolution-phase macrophages possess a unique inflammatory phenotype that is controlled by cAMP. Blood 112, 4117–4127 (2008). · DOI · Paper page
  67. Stables, M. J. et al. Transcriptomic analyses of murine resolution-phase macrophages. Blood 118, e192–e208 (2011). · DOI · Paper page
  68. Fredman, G. & Serhan, C. N. Specialized proresolving mediator targets for RvE1 and RvD1 in peripheral blood and mechanisms of resolution. Biochem. J. 437, 185–197 (2011). · DOI
  69. Galli, S. J., Nakae, S. & Tsai, M. Mast cells in the development of adaptive immune responses. Nat. Immunol. 6, 135–142 (2005). · DOI · Paper page
  70. Yu, Y., Blokhuis, B. R., Garssen, J. & Redegeld, F. A. Non-IgE mediated mast cell activation. Eur. J. Pharm. 778, 33–43 (2016). · DOI
  71. Costanza, M., Colombo, M. P. & Pedotti, R. Mast cells in the pathogenesis of multiple sclerosis and experimental autoimmune encephalomyelitis. Int. J. Mol. Sci. 13, 15107–15125 (2012). · DOI
  72. Bischoff, S. C. Role of mast cells in allergic and non-allergic immune responses: comparison of human and murine data. Nat. Rev. Immunol. 7, 93–104 (2007). · DOI · Paper page
  73. Dudeck, A. et al. Mast cells are key promoters of contact allergy that mediate the adjuvant effects of haptens. Immunity 34, 973–984 (2011). · DOI · Paper page
  74. Cecere, T. E., Todd, S. M. & Leroith, T. Regulatory T cells in arterivirus and coronavirus infections: do they protect against disease or enhance it? Viruses 4, 833–846 (2012). · DOI
  75. Li, G. et al. Coronavirus infections and immune responses. J. Med. Virol. 92, 424–432 (2020). · DOI · Paper page
  76. Zabetakis, I., Lordan, R., Norton, C. & Tsoupras, A. COVID-19: the inflammation link and the role of nutrition in potential mitigation. Nutrients 12, 1466 (2020). · DOI · Paper page
  77. Steinbach, E. C. & Plevy, S. E. The role of macrophages and dendritic cells in the initiation of inflammation in IBD. Inflamm. Bowel Dis. 20, 166–175 (2014). · DOI · Paper page
  78. Martinek, J., Wu, T. C., Cadena, D., Banchereau, J. & Palucka, K. Interplay between dendritic cells and cancer cells. Int. Rev. Cell Mol. Biol. 348, 179–215 (2019). · DOI
  79. Schuster, S., Hurrell, B. & Tacchini-Cottier, F. Crosstalk between neutrophils and dendritic cells: a context-dependent process. J. Leukoc. Biol. 94, 671–675 (2013). · DOI
  80. Angeli, V. & Randolph, G. J. Inflammation, lymphatic function, and dendritic cell migration. Lymphat Res. Biol. 4, 217–228 (2006). · DOI
  81. Salminen, A., Kaarniranta, K. & Kauppinen, A. The role of myeloid-derived suppressor cells (MDSC) in the inflammaging process. Ageing Res. Rev. 48, 1–10 (2018). · DOI
  82. Goh, C. C. et al. Hepatitis C virus-induced myeloid-derived suppressor cells suppress NK cell IFN-gamma production by altering cellular metabolism via arginase-1. J. Immunol. 196, 2283–2292 (2016). · DOI
  83. Gleich, G. J. The functions of eosinophils. Ann. Inst. Pasteur Immunol. 137D, 136–141 (1986).
  84. Knol, E. F. & Olszewski, M. Basophils and mast cells: underdog in immune regulation? Immunol. Lett. 138, 28–31 (2011). · DOI
  85. Gilmartin, L., Tarleton, C. A., Schuyler, M., Wilson, B. S. & Oliver, J. M. A comparison of inflammatory mediators released by basophils of asthmatic and control subjects in response to high-affinity IgE receptor aggregation. Int. Arch. Allergy Immunol. 145, 182–192 (2008). · doi:10.1159/000109287
  86. Silver, M. R. et al. IL-33 synergizes with IgE-dependent and IgE-independent agents to promote mast cell and basophil activation. Inflamm. Res 59, 207–218 (2010). · DOI
  87. Gleich, G. J., Adolphson, C. R. & Leiferman, K. M. The biology of the eosinophilic leukocyte. Annu. Rev. Med 44, 85–101 (1993). · DOI · Paper page
  88. Strandmark, J. et al. Eosinophils are required to suppress Th2 responses in Peyer’s patches during intestinal infection by nematodes. Mucosal Immunol. 10, 661–672 (2017). · DOI
  89. Tosello-Trampont, A., Surette, F. A., Ewald, S. E. & Hahn, Y. S. Immunoregulatory role of NK Cells in tissue inflammation and regeneration. Front. Immunol. 8, 301 (2017). · DOI
  90. Hofmann, U. et al. Activation of CD4+ T lymphocytes improves wound healing and survival after experimental myocardial infarction in mice. Circulation 125, 1652–1663 (2012). · DOI · Paper page
  91. Wu, Y., Antony, S., Meitzler, J. L. & Doroshow, J. H. Molecular mechanisms underlying chronic inflammation-associated cancers. Cancer Lett. 345, 164–173 (2014). · DOI · Paper page
  92. Back, M., Yurdagul, A. Jr, Tabas, I., Oorni, K. & Kovanen, P. T. Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities. Nat. Rev. Cardiol. 16, 389–406 (2019).
  93. Ding, N. et al. Mast cells are important regulator of acupoint sensitization via the secretion of tryptase, 5-hydroxytryptamine, and histamine. PLoS ONE 13, e0194022 (2018). · doi:10.1371/journal.pone.0194022
  94. Shi, G. P., Bot, I. & Kovanen, P. T. Reply: The complexity of substance P-mediated mast cell activation. Nat. Rev. Cardiol. 14, 124 (2017). · doi:10.1038/nrcardio.2016.213
  95. Oschatz, C. et al. Mast cells increase vascular permeability by heparin-initiated bradykinin formation in vivo. Immunity 34, 258–268 (2011). · DOI · Paper page
  96. Stoll, G. & Nieswandt, B. Thrombo-inflammation in acute ischaemic stroke - implications for treatment. Nat. Rev. Neurol. 15, 473–481 (2019). · DOI · Paper page
  97. Nissinen, L. & Kahari, V. M. Matrix metalloproteinases in inflammation. Biochim. Biophys. Acta 1840, 2571–2580 (2014). · DOI · Paper page
  98. Courtois, G. & Gilmore, T. D. Mutations in the NF-kappaB signaling pathway: implications for human disease. Oncogene 25, 6831–6843 (2006). · DOI · Paper page
  99. Koehne, C. H. & Dubois, R. N. COX-2 inhibition and colorectal cancer. Semin. Oncol. 31, 12–21 (2004). · DOI · Paper page
  100. Szlosarek, P. W. & Balkwill, F. R. Tumour necrosis factor alpha: a potential target for the therapy of solid tumours. Lancet Oncol. 4, 565–573 (2003). · DOI · Paper page
  101. Uceyler, N. et al. Tumor necrosis factor-alpha links heat and inflammation with Fabry pain. Mol. Genet. Metab. 127, 200–206 (2019). · doi:10.1016/j.ymgme.2019.05.009
  102. Jordan, S. C. et al. Interleukin-6, a cytokine critical to mediation of inflammation, autoimmunity and allograft rejection: therapeutic implications of IL-6 receptor blockade. Transplantation 101, 32–44 (2017). · DOI · Paper page
  103. Nguyen, D. P., Li, J. & Tewari, A. K. Inflammation and prostate cancer: the role of interleukin 6 (IL-6). BJU Int. 113, 986–992 (2014). · DOI · Paper page
  104. Lacy, P. Editorial: secretion of cytokines and chemokines by innate immune cells. Front. Immunol. 6, 190 (2015). · DOI
  105. Rani, A., Dasgupta, P. & Murphy, J. J. Prostate cancer: the role of inflammation and chemokines. Am. J. Pathol. 189, 2119–2137 (2019). · DOI
  106. Borroni, E. M., Savino, B., Bonecchi, R. & Locati, M. Chemokines sound the alarmin: The role of atypical chemokine in inflammation and cancer. Semin. Immunol. 38, 63–71 (2018). · DOI
  107. Proost, P. et al. Chemokine isoforms and processing in inflammation and immunity. J. Autoimmun. 85, 45–57 (2017). · DOI
  108. Lazennec, G. & Richmond, A. Chemokines and chemokine receptors: new insights into cancer-related inflammation. Trends Mol. Med. 16, 133–144 (2010). · DOI · Paper page
  109. Chen, K. et al. Chemokines in homeostasis and diseases. Cell Mol. Immunol. 15, 324–334 (2018). · DOI · Paper page
  110. Yoshimura, T. The production of monocyte chemoattractant protein-1 (MCP-1)/CCL2 in tumor microenvironments. Cytokine 98, 71–78 (2017). · DOI
  111. Yoshimura, T. The chemokine MCP-1 (CCL2) in the host interaction with cancer: a foe or ally? Cell Mol. Immunol. 15, 335–345 (2018). · DOI · Paper page
  112. Marquez-Curtis, L. A. & Janowska-Wieczorek, A. Enhancing the migration ability of mesenchymal stromal cells by targeting the SDF-1/CXCR4 axis. Biomed. Res. Int. 2013, 561098 (2013). · DOI · Paper page
  113. Daniel, S. K., Seo, Y. D. & Pillarisetty, V. G. The CXCL12-CXCR4/CXCR7 axis as a mechanism of immune resistance in gastrointestinal malignancies. Semin. Cancer Biol. 65, 176–188 (2020). · DOI · Paper page
  114. Klos, A., Wende, E., Wareham, K. J. & Monk, P. N. International union of basic and clinical pharmacology [corrected]. LXXXVII. complement peptide C5a, C4a, and C3a receptors. Pharm. Rev. 65, 500–543 (2013). · DOI · Paper page
  115. Orsini, F., De Blasio, D., Zangari, R., Zanier, E. R. & De Simoni, M. G. Versatility of the complement system in neuroinflammation, neurodegeneration and brain homeostasis. Front. Cell Neurosci. 8, 380 (2014). · DOI
  116. Koelman, D. L. H., Brouwer, M. C. & van de Beek, D. Targeting the complement system in bacterial meningitis. Brain 142, 3325–3337 (2019). · DOI
  117. Erdei, A., Andrasfalvy, M., Peterfy, H., Toth, G. & Pecht, I. Regulation of mast cell activation by complement-derived peptides. Immunol. Lett. 92, 39–42 (2004). · DOI
  118. Cain, S. A. & Monk, P. N. The orphan receptor C5L2 has high affinity binding sites for complement fragments C5a and C5a des-Arg(74). J. Biol. Chem. 277, 7165–7169 (2002). · DOI · Paper page
  119. Janatova, J. C3, C5 components and C3a, C4a, and C5a fragments of the complement system. Methods Enzymol. 162, 579–625 (1988). · doi:10.1016/0076-6879(88)62104-5
  120. Lopez-Lera, A. et al. Complement as a diagnostic tool in immunopathology. Semin Cell Dev. Biol. 85, 86–97 (2019). · DOI
  121. Morgan, B. P. & Harris, C. L. Complement, a target for therapy in inflammatory and degenerative diseases. Nat. Rev. Drug Disco. 14, 857–877 (2015). · DOI · Paper page
  122. Basil, M. C. & Levy, B. D. Specialized pro-resolving mediators: endogenous regulators of infection and inflammation. Nat. Rev. Immunol. 16, 51–67 (2016). · DOI · Paper page
  123. Williams, K. I. & Higgs, G. A. Eicosanoids and inflammation. J. Pathol. 156, 101–110 (1988). · DOI
  124. Serhan, C. N. Lipoxins and aspirin-triggered 15-epi-lipoxins are the first lipid mediators of endogenous anti-inflammation and resolution. Prostaglandins Leukot. Ess. Fat. Acids 73, 141–162 (2005). · DOI · Paper page
  125. Serhan, C. N., Chiang, N., Dalli, J. & Levy, B. D. Lipid mediators in the resolution of inflammation. Cold Spring Harb. Perspect. Biol. 7, a016311 (2014). · DOI · Paper page
  126. Withana, N. P. et al. Dual-modality activity-based probes as molecular imaging agents for vascular inflammation. J. Nucl. Med. 57, 1583–1590 (2016). · DOI
  127. Zayani, Y. et al. Inflammations mediators and circulating levels of matrix metalloproteinases: biomarkers of diabetes in tunisians metabolic syndrome patients. Cytokine 86, 47–52 (2016). · DOI
  128. Alameddine, H. S. & Morgan, J. E. Matrix metalloproteinases and tissue inhibitor of metalloproteinases in inflammation and fibrosis of skeletal muscles. J. Neuromuscul. Dis. 3, 455–473 (2016). · DOI
  129. Baranek, T. et al. Elastin receptor (spliced galactosidase) occupancy by elastin peptides counteracts proinflammatory cytokine expression in lipopolysaccharide-stimulated human monocytes through NF-kappaB down-regulation. J. Immunol. 179, 6184–6192 (2007). · DOI
  130. Maeno, T. et al. CD8+ T Cells are required for inflammation and destruction in cigarette smoke-induced emphysema in mice. J. Immunol. 178, 8090–8096 (2007). · DOI · Paper page
  131. Stoka, V., Turk, V. & Turk, B. Lysosomal cathepsins and their regulation in aging and neurodegeneration. Ageing Res. Rev. 32, 22–37 (2016). · DOI · Paper page
  132. van Kasteren, S. I. & Overkleeft, H. S. Endo-lysosomal proteases in antigen presentation. Curr. Opin. Chem. Biol. 23, 8–15 (2014). · doi:10.1016/j.cbpa.2014.08.011
  133. Ahmad, S. & Siddiqi, M. I. Insights from molecular modeling into the selective inhibition of cathepsin S by its inhibitor. J. Mol. Model 23, 92 (2017). · DOI
  134. Tang, Y. et al. Cathepsin B inhibition ameliorates the non-alcoholic steatohepatitis through suppressing caspase-1 activation. J. Physiol. Biochem. 74, 503–510 (2018). · DOI
  135. Pan, W. et al. Inhibition of Ctsk alleviates periodontitis and comorbid rheumatoid arthritis via downregulation of the TLR9 signalling pathway. J. Clin. Periodontol. 46, 286–296 (2019). · DOI
  136. Asagiri, M. et al. Cathepsin K-dependent toll-like receptor 9 signaling revealed in experimental arthritis. Science 319, 624–627 (2008). · DOI · Paper page
  137. Anderson, P. Post-transcriptional regulons coordinate the initiation and resolution of inflammation. Nat. Rev. Immunol. 10, 24–35 (2010). · DOI · Paper page
  138. Anel, R. & Kumar, A. Human endotoxemia and human sepsis: limits to the model. Crit. Care 9, 151–152 (2005). · DOI
  139. Hesse, D. G. et al. Cytokine appearance in human endotoxemia and primate bacteremia. Surg. Gynecol. Obstet. 166, 147–153 (1988).
  140. Mazumder, B., Sampath, P. & Fox, P. L. Regulation of macrophage ceruloplasmin gene expression: one paradigm of 3’-UTR-mediated translational control. Mol. Cells 20, 167–172 (2005). · DOI
  141. Mazumder, B. et al. Regulated release of L13a from the 60S ribosomal subunit as a mechanism of transcript-specific translational control. Cell 115, 187–198 (2003). · DOI · Paper page
  142. Muhl, H. & Pfeilschifter, J. Anti-inflammatory properties of pro-inflammatory interferon-gamma. Int. Immunopharmacol. 3, 1247–1255 (2003). · DOI · Paper page
  143. Mazumder, B., Mukhopadhyay, C. K., Prok, A., Cathcart, M. K. & Fox, P. L. Induction of ceruloplasmin synthesis by IFN-gamma in human monocytic cells. J. Immunol. 159, 1938–1944 (1997). · DOI
  144. Serhan, C. N. et al. Resolvins: a family of bioactive products of omega-3 fatty acid transformation circuits initiated by aspirin treatment that counter proinflammation signals. J. Exp. Med. 196, 1025–1037 (2002). · DOI · Paper page
  145. Serhan, C. N. & Chiang, N. Novel endogenous small molecules as the checkpoint controllers in inflammation and resolution: entree for resoleomics. Rheum. Dis. Clin. North Am. 30, 69–95 (2004). · DOI
  146. Schwab, J. M., Chiang, N., Arita, M. & Serhan, C. N. Resolvin E1 and protectin D1 activate inflammation-resolution programmes. Nature 447, 869–874 (2007). · DOI · Paper page
  147. O’Meara, S. J., Rodgers, K. & Godson, C. Lipoxins: update and impact of endogenous pro-resolution lipid mediators. Rev. Physiol. Biochem. Pharm. 160, 47–70 (2008).
  148. Serhan, C. N. Lipoxins and aspirin-triggered 15-epi-lipoxin biosynthesis: an update and role in anti-inflammation and pro-resolution. Prostaglandins Other Lipid Mediat 68-69, 433–455 (2002). · DOI · Paper page
  149. Serhan, C. N., Hamberg, M. & Samuelsson, B. Lipoxins: novel series of biologically active compounds formed from arachidonic acid in human leukocytes. Proc. Natl Acad. Sci. USA 81, 5335–5339 (1984). · DOI · Paper page
  150. Serhan, C. N., Arita, M., Hong, S. & Gotlinger, K. Resolvins, docosatrienes, and neuroprotectins, novel omega-3-derived mediators, and their endogenous aspirin-triggered epimers. Lipids 39, 1125–1132 (2004). · DOI · Paper page
  151. Serhan, C. N., Gotlinger, K., Hong, S. & Arita, M. Resolvins, docosatrienes, and neuroprotectins, novel omega-3-derived mediators, and their aspirin-triggered endogenous epimers: an overview of their protective roles in catabasis. Prostaglandins Other Lipid Mediat. 73, 155–172 (2004). · DOI · Paper page
  152. Eickmeier, O. et al. Aspirin-triggered resolvin D1 reduces mucosal inflammation and promotes resolution in a murine model of acute lung injury. Mucosal Immunol. 6, 256–266 (2013). · DOI · Paper page
  153. Samson, M. et al. ChemR23, a putative chemoattractant receptor, is expressed in monocyte-derived dendritic cells and macrophages and is a coreceptor for SIV and some primary HIV-1 strains. Eur. J. Immunol. 28, 1689–1700 (1998). · DOI · Paper page
  154. Payrits, M. et al. Resolvin D1 and D2 inhibit transient receptor potential Vanilloid 1 and Ankyrin 1 ion channel activation on sensory neurons via lipid raft modification. Int. J. Mol. Sci. 21, 5019 (2020). · DOI
  155. Chiang, N., Dalli, J., Colas, R. A. & Serhan, C. N. Identification of resolvin D2 receptor mediating resolution of infections and organ protection. J. Exp. Med 212, 1203–1217 (2015). · DOI · Paper page
  156. Back, M. & Hansson, G. K. Omega-3 fatty acids, cardiovascular risk, and the resolution of inflammation. FASEB J. 33, 1536–1539 (2019). · DOI
  157. Lopez-Vicario, C. et al. Association of a variant in the gene encoding for ERV1/ChemR23 with reduced inflammation in visceral adipose tissue from morbidly obese individuals. Sci. Rep. 7, 15724 (2017). · DOI · Paper page
  158. Zhou, Y. et al. Fibrinogen-like protein 2 controls sepsis catabasis by interacting with resolvin Dp5. Sci. Adv. 5, eaax0629 (2019). · DOI
  159. Marcheselli, V. L. et al. Neuroprotectin D1/protectin D1 stereoselective and specific binding with human retinal pigment epithelial cells and neutrophils. Prostaglandins Leukot. Ess. Fat. Acids 82, 27–34 (2010). · DOI
  160. Kohli, P. & Levy, B. D. Resolvins and protectins: mediating solutions to inflammation. Br. J. Pharm. 158, 960–971 (2009). · DOI · Paper page
  161. Serhan, C. N. et al. Anti-inflammatory actions of neuroprotectin D1/protectin D1 and its natural stereoisomers: assignments of dihydroxy-containing docosatrienes. J. Immunol. 176, 1848–1859 (2006). · DOI · Paper page
  162. Chiurchiu, V. et al. Proresolving lipid mediators resolvin D1, resolvin D2, and maresin 1 are critical in modulating T cell responses. Sci. Transl. Med. 8, 353ra111 (2016). · DOI · Paper page
  163. Chatterjee, A. et al. The pro-resolving lipid mediator maresin 1 (MaR1) attenuates inflammatory signaling pathways in vascular smooth muscle and endothelial cells. PLoS ONE 9, e113480 (2014). · DOI
  164. Hong, S. et al. Maresin-like lipid mediators are produced by leukocytes and platelets and rescue reparative function of diabetes-impaired macrophages. Chem. Biol. 21, 1318–1329 (2014). · DOI
  165. Liening, S., Romp, E., Werz, O., Scriba, G. K. E. & Garscha, U. Liquid chromatography-coupled mass spectrometry analysis of glutathione conjugates of oxygenated polyunsaturated fatty acids. Prostaglandins Other Lipid Mediat. 144, 106350 (2019). · DOI
  166. Liu, Y. J. et al. PCTR1 ameliorates lipopolysaccharide-induced acute inflammation and multiple organ damage via regulation of linoleic acid metabolism by promoting FADS1/FASDS2/ELOV2 expression and reducing PLA2 expression. Lab. Invest. 100, 904–915 (2020). · DOI
  167. Ramon, S. et al. The protectin PCTR1 is produced by human M2 macrophages and enhances resolution of infectious inflammation. Am. J. Pathol. 186, 962–973 (2016). · DOI
  168. Zhang, Q., Zhu, B. & Li, Y. Resolution of cancer-promoting inflammation: a new approach for anticancer therapy. Front. Immunol. 8, 71 (2017).
  169. Xian, W. et al. The pro-resolving lipid mediator maresin 1 protects against cerebral ischemia/reperfusion injury by attenuating the pro-inflammatory response. Biochem. Biophys. Res. Commun. 472, 175–181 (2016). · DOI
  170. Hwang, S. M., Chung, G., Kim, Y. H. & Park, C. K. The role of maresins in inflammatory pain: function of macrophages in wound regeneration. Int. J. Mol. Sci. 20, 5849 (2019). · DOI
  171. Serhan, C. N., Chiang, N. & Dalli, J. New pro-resolving n-3 mediators bridge resolution of infectious inflammation to tissue regeneration. Mol. Asp. Med. 64, 1–17 (2018). · DOI · Paper page
  172. Chiang, N. et al. New maresin conjugates in tissue regeneration pathway counters leukotriene D4-stimulated vascular responses. FASEB J. 32, 4043–4052 (2018). · DOI
  173. de la Rosa, X. et al. Identification and complete stereochemical assignments of the new resolvin conjugates in tissue regeneration in human tissues that stimulate proresolving phagocyte functions and tissue regeneration. Am. J. Pathol. 188, 950–966 (2018). · DOI
  174. Flesher, R. P., Herbert, C. & Kumar, R. K. Resolvin E1 promotes resolution of inflammation in a mouse model of an acute exacerbation of allergic asthma. Clin. Sci. 126, 805–814 (2014). · DOI
  175. Wang, X. et al. Resolution of inflammation is altered in Alzheimer’s disease. Alzheimers Dement. 11, 40–50 (2015). e41-42. · DOI · Paper page
  176. Yang, L. et al. Immune characteristics of severe and critical COVID-19 patients. Signal Transduct. Target Ther. 5, 179 (2020). · doi:10.1038/s41392-020-00296-3
  177. Mehta, P. et al. COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet 395, 1033–1034 (2020). · DOI · Paper page
  178. Rokni, M., Hamblin, M. R. & Rezaei, N. Cytokines and COVID-19: friends or foes? Hum. Vaccin Immunother. 16, 2363–2365 (2020). · DOI
  179. Otsuka, R. & Seino, K. I. Macrophage activation syndrome and COVID-19. Inflamm. Regen. 40, 19 (2020). · DOI
  180. Das, U. N. Can bioactive lipids inactivate coronavirus (COVID-19)? Arch. Med. Res. 51, 282–286 (2020). · DOI · Paper page
  181. Fekete, T. et al. Regulatory NLRs control the RLR-mediated Type I interferon and inflammatory responses in human dendritic cells. Front. Immunol. 9, 2314 (2018). · DOI
  182. Si, Y. et al. Posttranslational modification control of inflammatory signaling. Adv. Exp. Med. Biol. 1024, 37–61 (2017). · DOI
  183. Istomin, A. Y. & Godzik, A. Understanding diversity of human innate immunity receptors: analysis of surface features of leucine-rich repeat domains in NLRs and TLRs. BMC Immunol. 10, 48 (2009). · DOI
  184. Dolasia, K., Bisht, M. K., Pradhan, G., Udgata, A. & Mukhopadhyay, S. TLRs/NLRs: shaping the landscape of host immunity. Int. Rev. Immunol. 37, 3–19 (2018). · DOI
  185. Broad, A., Kirby, J. A., Jones, D. E., Applied, I. & Transplantation Research, G. Toll-like receptor interactions: tolerance of MyD88-dependent cytokines but enhancement of MyD88-independent interferon-beta production. Immunology 120, 103–111 (2007). · DOI
  186. Wieland, C. W. et al. The MyD88-dependent, but not the MyD88-independent, pathway of TLR4 signaling is important in clearing nontypeable haemophilus influenzae from the mouse lung. J. Immunol. 175, 6042–6049 (2005). · DOI
  187. Triantafilou, M. et al. Membrane sorting of toll-like receptor (TLR)-2/6 and TLR2/1 heterodimers at the cell surface determines heterotypic associations with CD36 and intracellular targeting. J. Biol. Chem. 281, 31002–31011 (2006). · DOI · Paper page
  188. Bagchi, A. et al. MyD88-dependent and MyD88-independent pathways in synergy, priming, and tolerance between TLR agonists. J. Immunol. 178, 1164–1171 (2007). · DOI · Paper page
  189. Tamassia, N. et al. The MyD88-independent pathway is not mobilized in human neutrophils stimulated via TLR4. J. Immunol. 178, 7344–7356 (2007). · DOI
  190. Karnati, H. K. et al. TLR-4 signalling pathway: MyD88 independent pathway up-regulation in chicken breeds upon LPS treatment. Vet. Res. Commun. 39, 73–78 (2015). · DOI
  191. Inohara, N. & Nunez, G. NODs: intracellular proteins involved in inflammation and apoptosis. Nat. Rev. Immunol. 3, 371–382 (2003). · DOI · Paper page
  192. Chamaillard, M., Girardin, S. E., Viala, J. & Philpott, D. J. Nods, Nalps and Naip: intracellular regulators of bacterial-induced inflammation. Cell Microbiol. 5, 581–592 (2003). · DOI · Paper page
  193. Ting, J. P. et al. The NLR gene family: a standard nomenclature. Immunity 28, 285–287 (2008). · DOI · Paper page
  194. Wagner, R. N., Proell, M., Kufer, T. A. & Schwarzenbacher, R. Evaluation of Nod-like receptor (NLR) effector domain interactions. PLoS ONE 4, e4931 (2009). · DOI
  195. Schroder, K. & Tschopp, J. The inflammasomes. Cell 140, 821–832 (2010). · DOI · Paper page
  196. Man, S. M., Karki, R. & Kanneganti, T. D. Molecular mechanisms and functions of pyroptosis, inflammatory caspases and inflammasomes in infectious diseases. Immunol. Rev. 277, 61–75 (2017). · DOI · Paper page
  197. Xue, Y., Enosi Tuipulotu, D., Tan, W. H., Kay, C. & Man, S. M. Emerging activators and regulators of inflammasomes and pyroptosis. Trends Immunol. 40, 1035–1052 (2019). · DOI · Paper page
  198. Feng, S., Fox, D. & Man, S. M. Mechanisms of gasdermin family members in inflammasome signaling and cell death. J. Mol. Biol. 430, 3068–3080 (2018). · DOI · Paper page
  199. Kanneganti, A. et al. GSDMD is critical for autoinflammatory pathology in a mouse model of Familial Mediterranean Fever. J. Exp. Med. 215, 1519–1529 (2018). · DOI · Paper page
  200. Xiao, J. et al. Gasdermin D mediates the pathogenesis of neonatal-onset multisystem inflammatory disease in mice. PLoS Biol. 16, e3000047 (2018). · DOI

200 of 787 shown

Cited by

See all 2,792

Metadata

Authors
Zhao, H., Wu, L., Yan, G., Chen, Y., Zhou, M., Wu, Y., & Li, Y.
Venue
Signal Transduction and Targeted Therapy
Published
2021-07-12
Volume
6
Issue
1
Pages
263-263
ISSN
2059-3635 (ISSN-L)
OpenAlex
W3180882235
Cited by
2,792
References
119
FWCI
106.80
Type
journal article
Language
en
Open access
gold
Licence
Funders
National Science Foundation of China | Major International Joint Research Programme (81920108027)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: Inflammation and tumor progression: signaling pathways and targeted intervention. https://app.cochat.ai/papers/10.1038/s41392-021-00658-5
The paper
Zhao, H., Wu, L., Yan, G., Chen, Y., Zhou, M., Wu, Y., & Li, Y. (2021). Inflammation and tumor progression: signaling pathways and targeted intervention. Signal Transduction and Targeted Therapy. https://doi.org/10.1038/s41392-021-00658-5

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.