Suppression of lung adenocarcinoma progression by Nkx2-1

Monte M. Winslow, Talya L. Dayton, Roel G. W. Verhaak, Caroline Kim-Kiselak, Eric L. Snyder, David M. Feldser, Diana D. Hubbard, Michel J. DuPage, Charles A. Whittaker, Sebastian Hoersch, Stephanie Yoon, Denise Crowley, Roderick T. Bronson, Derek Y. Chiang, Matthew Meyerson and Tyler Jacks ()
Additional contact information
Monte M. Winslow: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Talya L. Dayton: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Roel G. W. Verhaak: Dana-Farber Cancer Institute, Harvard University
Caroline Kim-Kiselak: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Eric L. Snyder: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
David M. Feldser: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Diana D. Hubbard: Dana-Farber Cancer Institute, Harvard University
Michel J. DuPage: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Charles A. Whittaker: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Sebastian Hoersch: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Stephanie Yoon: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Denise Crowley: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
Roderick T. Bronson: Tufts University Veterinary School
Derek Y. Chiang: Dana-Farber Cancer Institute, Harvard University
Matthew Meyerson: Dana-Farber Cancer Institute, Harvard University
Tyler Jacks: David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology

Nature, 2011, vol. 473, issue 7345, 101-104

Abstract: Nkx2-1 as an oncogene and tumour-suppressor In a mouse model of lung cancer driven by activated K-Ras and p53 loss, Jacks and colleagues describe a method for tracing individual metastases back to the primary tumours, allowing non-metastatic lesions to be distinguished from metastatic lesions in the same animal. A comparison of gene-expression signatures between metastatic and non-metastatic tumours with human lung cancers led to the identification of Nkx2-1/TTF-1 as a gene that is down-regulated during tumour progression in mice, and associated with poorer outcome in patients. Nkx2-1 loss promotes metastasis at least in part by regulating Hmga2, resulting in de-differentiation. Thus Nkx2-1, previously identified as a lung-cancer oncogene, can also function as a suppressor of lung-cancer progression.

Date: 2011
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DOI: 10.1038/nature09881

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