作者: Anita L. Ray , Eliseo F. Castillo , Katherine T. Morris , Robert A. Nofchissey , Lea L. Weston
DOI: 10.1002/IJC.29716
关键词:
摘要: Chronic inflammation is a risk factor for colorectal cancer. The MAPK-activated protein kinase 2 (MK2) pathway controls multiple cellular processes including p38-dependent inflammation. This the first study to investigate role of MK2 in development colitis-associated colon cancer (CAC). Herein, we demonstrate that MK2(-/-) mice are highly resistant neoplasm when exposed AOM/DSS, while wild type (WT) C57BL/6 develop neoplasms with same treatment. MK2-specific cytokines IL-1, IL-6 and TNF-α were substantially decreased AOM/DSS treated mouse tissues compared WT mice, which coincided marked decrease macrophage influx. Restoring MK2-competent macrophages by injecting bone marrow derived into led partial restoration inflammatory cytokine production treatment; however, not sufficient induce development. These results indicate functions as an regulator promote colonic may be potential target CAC.