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Targeting filamin A reduces K-RAS-induced lung adenocarcinomas and endothelial response to tumor growth in mice
University of Gothenburg, Sweden University of Gothenburg, Sweden .
University of Gothenburg, Sweden University of Gothenburg, Sweden .
University of Gothenburg, Sweden University of Gothenburg, Sweden .
University of Gothenburg, Sweden University of Gothenburg, Sweden .
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2012 (English)In: Molecular Cancer, ISSN 1476-4598, E-ISSN 1476-4598, Vol. 11, no 50Article in journal (Refereed) Published
Abstract [en]

Background: Many human cancer cells express filamin A (FLNA), an actin-binding structural protein that interacts with a diverse set of cell signaling proteins, but little is known about the biological importance of FLNA in tumor development. FLNA is also expressed in endothelial cells, which may be important for tumor angiogenesis. In this study, we defined the impact of targeting Flna in cancer and endothelial cells on the development of tumors in vivo and on the proliferation of fibroblasts in vitro. less thanbrgreater than less thanbrgreater thanMethods: First, we used a Cre-adenovirus to simultaneously activate the expression of oncogenic K-RAS and inactivate the expression of Flna in the lung and in fibroblasts. Second, we subcutaneously injected mouse fibrosarcoma cells into mice lacking Flna in endothelial cells. less thanbrgreater than less thanbrgreater thanResults: Knockout of Flna significantly reduced K-RAS-induced lung tumor formation and the proliferation of oncogenic K-RAS-expressing fibroblasts, and attenuated the activation of the downstream signaling molecules ERK and AKT. Genetic deletion of endothelial FLNA in mice did not impact cardiovascular development; however, knockout of Flna in endothelial cells reduced subcutaneous fibrosarcoma growth and vascularity within tumors. less thanbrgreater than less thanbrgreater thanConclusions: We conclude that FLNA is important for lung tumor growth and that endothelial Flna impacts local tumor growth. The data shed new light on the biological importance of FLNA and suggest that targeting this protein might be useful in cancer therapeutics.

Place, publisher, year, edition, pages
BioMed Central , 2012. Vol. 11, no 50
Keyword [en]
Cancer, Angiogenesis, Cytoskeleton, Migration
National Category
Engineering and Technology
Identifiers
URN: urn:nbn:se:liu:diva-84539DOI: 10.1186/1476-4598-11-50ISI: 000308749900001OAI: oai:DiVA.org:liu-84539DiVA: diva2:560162
Note

Funding Agencies|The Swedish Society of Medicine||The Assar Gabrielsson Foundation||The Sahlgrenska University Hospital||The Swedish Research Council||The Swedish Cancer Society||

Available from: 2012-10-12 Created: 2012-10-12 Last updated: 2017-12-07Bibliographically approved

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