ERK5 is a critical mediator of inflammation-driven cancer

  • Finegan K
  • Perez-Madrigal D
  • Hitchin J
 et al. 
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Abstract

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.

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Authors

  • allan jordanCancer Research UK Manchester Institute

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  • Katherine G. Finegan

  • Diana Perez-Madrigal

  • James R. Hitchin

  • Clare C. Davies

  • Cathy Tournier

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