Original Paper

Oncogene (2005) 24, 3397–3408. doi:10.1038/sj.onc.1208469 Published online 28 February 2005

Stat3 regulates genes common to both wound healing and cancer

Daniel J Dauer1,3, Bernadette Ferraro1,3, Lanxi Song1,3, Bin Yu1,3, Linda Mora2,3, Ralf Buettner2,3, Steve Enkemann2,3, Richard Jove2,3 and Eric B Haura1,3

  1. 1Thoracic Oncology/Experimental Therapeutics, H Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA
  2. 2Molecular Oncology Programs, H Lee Moffitt Cancer Center and Research Institute, Tampa, FL 33612, USA
  3. 3Department of Interdisciplinary Oncology, University of South Florida College of Medicine, Tampa, FL 33612, USA

Correspondence: EB Haura, Thoracic Oncology and Experimental Therapeutics Programs, H Lee Moffitt Cancer Center and Research Institute, MRC3 East, Room 3056, 12902 Magnolia Drive, Tampa, FL 33612-9497, USA. E-mail: hauraeb@moffitt.usf.edu

Received 10 November 2004; Revised 8 December 2004; Accepted 20 December 2004; Published online 28 February 2005.

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Abstract

Wound healing and cancer are both characterized by cell proliferation, remodeling of extracellular matrix, cell invasion and migration, new blood vessel formation, and modulation of blood coagulation. The mechanisms that link wound healing and cancer are poorly understood. We report here that Stat3, a common signaling mechanism involved in oncogenesis and tissue injury, regulates a common set of genes involved in wound healing and cancer. Using oligonucleotide gene arrays and quantitative real-time PCR, we evaluated changes in global gene expression resulting from expression of Stat3 in lung epithelial cells. We report here previously uncharacterized genes induced by Stat3 implicated in signaling pathways common to both wound healing and cancer including cell invasion and migration, angiogenesis, modulation of coagulation, and repression of interferon-inducible genes. Consistent with these results, we found increased Stat3 activity associated with wound healing in chronically inflamed mouse lungs and increased Stat3 activity was identified at the leading edge of lung tumors invading adjacent nontumor stroma. These findings provide a molecular basis for understanding cancer as a deregulation of normal wound healing processes.

Keywords:

STAT proteins, cancer, wound healing, Stat3, lung cancer

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