ERK5 is a critical mediator of inflammation-driven cancer

Research output: Contribution to journalArticle


  • Katherine G Finegan
  • Diana Perez-Madrigal
  • James R Hitchin
  • Allan M Jordan
  • Cathy Tournier

Colleges, School and Institutes


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)742-53
Number of pages12
JournalCancer Research
Issue number4
Early online date3 Feb 2015
Publication statusPublished - 15 Feb 2015


  • Animals, Carcinogenesis, Carcinogens, Epidermis, Gene Expression Regulation, Neoplastic, Humans, Inflammation, Keratinocytes, Mice, Mice, Transgenic, Mitogen-Activated Protein Kinase 7, Skin Neoplasms