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We have identified the MAPK\u2010activated protein kinase 2 (MK2) pathway as a primary mediator of inflammation in CRC. MK2 signaling promotes production of proinflammatory cytokines IL\u20101\u03b2, IL\u20106 and TNF\u2010\u03b1. These cytokines have been implicated in tumor growth, invasion and metastasis. For the first time, we investigate whether MK2 inhibition can improve outcome in two mouse models of CRC. In our azoxymethane\/dextran sodium sulfate (AOM\/DSS) model of colitis\u2010associated CRC, MK2 inhibitor treatment eliminated murine tumor development. Using the implanted, syngeneic murine CRC cell line CT26, we observe significant tumor volume reduction following MK2 inhibition. Tumor cells treated with MK2 inhibitors produced 80% less IL\u20101\u03b2, IL\u20106 and TNF\u2010\u03b1 and demonstrated decreased invasion. Replenishment of downstream proinflammatory MK2\u2010mediated cytokines (IL\u20101\u03b2, IL\u20106 and TNF\u2010\u03b1) to tumors led to restoration of tumor proliferation and rapid tumor regrowth. These results demonstrate the importance of MK2 in driving proinflammatory cytokine production, its relevance to\n                    <jats:italic>in vivo<\/jats:italic>\n                    tumor proliferation and invasion. Inhibition of MK2 may represent an attractive therapeutic target to suppress tumor growth and progression in patients.\n                  <\/jats:p>","DOI":"10.1002\/ijc.31191","type":"journal-article","created":{"date-parts":[[2017,12,2]],"date-time":"2017-12-02T03:16:44Z","timestamp":1512184604000},"page":"1702-1711","source":"Crossref","is-referenced-by-count":78,"title":["Inhibition of MK2 suppresses IL\u20101\u03b2, IL\u20106, and TNF\u2010\u03b1\u2010dependent colorectal cancer growth"],"prefix":"10.1002","volume":"142","author":[{"given":"Anita L.","family":"Ray","sequence":"first","affiliation":[{"name":"Department of Molecular Genetics and Microbiology University of New Mexico Health Sciences Center Albuquerque New Mexico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kiersten L.","family":"Berggren","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Medical Oncology Section of Radiation Oncology, University of New 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