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Forkhead box F1 regulates tumor-promoting properties of cancer-associated fibroblasts in lung cancer
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology. (Johan Botling)
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2010 (English)In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 70, no 7, 2644-2654 p.Article in journal (Refereed) Published
Abstract [en]

Cancer-associated fibroblasts (CAF) attract increasing attention as potential cancer drug targets due to their ability to stimulate, for example, tumor growth, invasion, angiogenesis, and metastasis. However, the molecular mechanisms causing the tumor-promoting properties of CAFs remain poorly understood. Forkhead box F1 (FoxF1) is a mesenchymal target of hedgehog signaling, known to regulate mesenchymal-epithelial interactions during lung development. Studies with FoxF1 gain- and loss-of-function fibroblasts revealed that FoxF1 regulates the contractility of fibroblasts, their production of hepatocyte growth factor and fibroblast growth factor-2, and their stimulation of lung cancer cell migration. FoxF1 status of fibroblasts was also shown to control the ability of fibroblasts to stimulate xenografted tumor growth. FoxF1 was expressed in CAFs of human lung cancer and associated with activation of hedgehog signaling. These observations suggest that hedgehog-dependent FoxF1 is a clinically relevant lung CAF-inducing factor, and support experimentally the general concept that CAF properties can be induced by activation of developmentally important transcription factors.

Place, publisher, year, edition, pages
2010. Vol. 70, no 7, 2644-2654 p.
Keyword [en]
Forkhead box F1
National Category
Respiratory Medicine and Allergy Cell and Molecular Biology
Research subject
Lung Medicine; Pathology
URN: urn:nbn:se:uu:diva-125768DOI: 10.1158/0008-5472.CAN-09-3644ISI: 000278486000010PubMedID: 20233876OAI: oai:DiVA.org:uu-125768DiVA: diva2:321002
Available from: 2010-05-28 Created: 2010-05-28 Last updated: 2010-12-17Bibliographically approved

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