| First Author | Finegan KG | Year | 2015 |
| Journal | Cancer Res | Volume | 75 |
| Issue | 4 | Pages | 742-53 |
| PubMed ID | 25649771 | Mgi Jnum | J:219957 |
| Mgi Id | MGI:5630022 | Doi | 10.1158/0008-5472.CAN-13-3043 |
| Citation | Finegan KG, et al. (2015) ERK5 is a critical mediator of inflammation-driven cancer. Cancer Res 75(4):742-53 |
| abstractText | Chronic inflammation is a hallmark of many cancers, yet the pathogenic mechanisms that distinguish cancer-associated inflammation from benign persistent inflammation are still mainly unclear. Here, we report that the protein kinase ERK5 controls the expression of a specific subset of inflammatory mediators in the mouse epidermis, which triggers the recruitment of inflammatory cells needed to support skin carcinogenesis. Accordingly, inactivation of ERK5 in keratinocytes prevents inflammation-driven tumorigenesis in this model. In addition, we found that anti-ERK5 therapy cooperates synergistically with existing antimitotic regimens, enabling efficacy of subtherapeutic doses. Collectively, our findings identified ERK5 as a mediator of cancer-associated inflammation in the setting of epidermal carcinogenesis. Considering that ERK5 is expressed in almost all tumor types, our findings suggest that targeting tumor-associated inflammation via anti-ERK5 therapy may have broad implications for the treatment of human tumors. |
