ERK5 is a critical mediator of inflammation-driven cancer.

Katherine Finegan, Diana Perez Madrigal, James Hitchin, Clare Davies, Allan Jordan, Cathy Tournier

Research output: Contribution to journalArticlepeer-review


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.
Original languageEnglish
Pages (from-to)742-753
JournalCancer Research
Issue number4
Publication statusPublished - 15 Feb 2015


Dive into the research topics of 'ERK5 is a critical mediator of inflammation-driven cancer.'. Together they form a unique fingerprint.

Cite this