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LEE, K.-S; LEE, Y.-S; WEE, H; LEE, H.-W; HOSOYA, A; CHUNG, J.-H; JANG, J.-J; KUNDU, J. K; SURH, Y.-J; KIM, W.-J; ITO, Y; JUNG, H.-S; LEE, J.-M; BAE, S.-C; ITO, K; CINGHU, S; KIM, J.-H; JANG, J.-W; LI, Y.-H; GOH, Y.-M; CHI, X.-Z
Oncogene, 06/2010, Letnik: 29, Številka: 23Journal Article
Human lung adenocarcinoma, the most prevalent form of lung cancer, is characterized by many molecular abnormalities. K-ras mutations are associated with the initiation of lung adenocarcinomas, but K-ras-independent mechanisms may also initiate lung tumors. Here, we find that the runt-related transcription factor Runx3 is essential for normal murine lung development and is a tumor suppressor that prevents lung adenocarcinoma. Runx3-/- mice, which die soon after birth, exhibit alveolar hyperplasia. Importantly, Runx3-/- bronchioli exhibit impaired differentiation, as evidenced by the accumulation of epithelial cells containing specific markers for both alveolar (that is SP-B) and bronchiolar (that is CC10) lineages. Runx3-/- epithelial cells also express Bmi1, which supports self-renewal of stem cells. Lung adenomas spontaneously develop in aging Runx3+/- mice ( approximately 18 months after birth) and invariably exhibit reduced levels of Runx3. As K-ras mutations are very rare in these adenomas, Runx3+/- mice provide an animal model for lung tumorigenesis that recapitulates the preneoplastic stage of human lung adenocarcinoma development, which is independent of K-Ras mutation. We conclude that Runx3 is essential for lung epithelial cell differentiation, and that downregulation of Runx3 is causally linked to the preneoplastic stage of lung adenocarcinoma.
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in: SICRIS
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