Activin enhances skin tumourigenesis and malignant progression by inducing a pro-tumourigenic immune cell response

Maria Antsiferova, Marcel Huber, Michael Meyer, Aleksandra Piwko-Czuchra, Tamara Ramadan, Amanda S. MacLeod, Wendy L. Havran, Reinhard Dummer, Daniel Hohl and Sabine Werner ()
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Maria Antsiferova: Institute of Cell Biology, ETH Zurich, 8093 Zurich, Switzerland.
Marcel Huber: University of Lausanne, 1011 Lausanne, Switzerland.
Michael Meyer: Institute of Cell Biology, ETH Zurich, 8093 Zurich, Switzerland.
Aleksandra Piwko-Czuchra: Institute of Cell Biology, ETH Zurich, 8093 Zurich, Switzerland.
Tamara Ramadan: Institute of Cell Biology, ETH Zurich, 8093 Zurich, Switzerland.
Amanda S. MacLeod: The Scripps Research Institute, La Jolla, California 92037, USA.
Wendy L. Havran: The Scripps Research Institute, La Jolla, California 92037, USA.
Reinhard Dummer: University Hospital, 8091 Zurich, Switzerland.
Daniel Hohl: University of Lausanne, 1011 Lausanne, Switzerland.
Sabine Werner: Institute of Cell Biology, ETH Zurich, 8093 Zurich, Switzerland.

Nature Communications, 2011, vol. 2, issue 1, 1-10

Abstract: Abstract Activin is an important orchestrator of wound repair, but its potential role in skin carcinogenesis has not been addressed. Here we show using different types of genetically modified mice that enhanced levels of activin in the skin promote skin tumour formation and their malignant progression through induction of a pro-tumourigenic microenvironment. This includes accumulation of tumour-promoting Langerhans cells and regulatory T cells in the epidermis. Furthermore, activin inhibits proliferation of tumour-suppressive epidermal γδ T cells, resulting in their progressive loss during tumour promotion. An increase in activin expression was also found in human cutaneous basal and squamous cell carcinomas when compared with control tissue. These findings highlight the parallels between wound healing and cancer, and suggest inhibition of activin action as a promising strategy for the treatment of cancers overexpressing this factor.

Date: 2011
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DOI: 10.1038/ncomms1585

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