| First Author | Ray AL | Year | 2016 |
| Journal | Int J Cancer | Volume | 138 |
| Issue | 3 | Pages | 770-5 |
| PubMed ID | 26238259 | Mgi Jnum | J:227929 |
| Mgi Id | MGI:5704018 | Doi | 10.1002/ijc.29716 |
| Citation | Ray AL, et al. (2016) Blockade of MK2 is protective in inflammation-associated colorectal cancer development. Int J Cancer 138(3):770-5 |
| abstractText | 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 is the first study to investigate the role of MK2 in development of colitis-associated colon cancer (CAC). Herein, we demonstrate that MK2(-/-) mice are highly resistant to neoplasm development when exposed to AOM/DSS, while wild type (WT) C57BL/6 develop multiple neoplasms with the same treatment. MK2-specific cytokines IL-1, IL-6 and TNF-alpha were substantially decreased in AOM/DSS treated MK2(-/-) mouse colon tissues compared with WT mice, which coincided with a marked decrease in macrophage influx. Restoring MK2-competent macrophages by injecting WT bone marrow derived macrophages into MK2(-/-) mice led to partial restoration of inflammatory cytokine production with AOM/DSS treatment; however, macrophages were not sufficient to induce neoplasm development. These results indicate that MK2 functions as an inflammatory regulator to promote colonic neoplasm development and may be a potential target for CAC. |
