Cited 67 times in
Runx3 is required for the differentiation of lung epithelial cells and suppression of lung cancer.
DC Field | Value | Language |
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dc.contributor.author | 이종민 | - |
dc.contributor.author | 정한성 | - |
dc.date.accessioned | 2015-04-23T16:46:51Z | - |
dc.date.available | 2015-04-23T16:46:51Z | - |
dc.date.issued | 2010 | - |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/101212 | - |
dc.description.abstract | 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 | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 3349~3361 | - |
dc.relation.isPartOf | ONCOGENE | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Adenocarcinoma/etiology | - |
dc.subject.MESH | Adenocarcinoma/pathology | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Cell Differentiation | - |
dc.subject.MESH | Cell Proliferation | - |
dc.subject.MESH | Core Binding Factor Alpha 3 Subunit/deficiency | - |
dc.subject.MESH | Core Binding Factor Alpha 3 Subunit/genetics | - |
dc.subject.MESH | Core Binding Factor Alpha 3 Subunit/physiology* | - |
dc.subject.MESH | Epithelial Cells/cytology | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Lung/cytology* | - |
dc.subject.MESH | Lung Neoplasms/etiology | - |
dc.subject.MESH | Lung Neoplasms/pathology | - |
dc.subject.MESH | Lung Neoplasms/prevention & control* | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Mice, Inbred C57BL | - |
dc.subject.MESH | Nuclear Proteins/analysis | - |
dc.subject.MESH | Nuclear Proteins/physiology | - |
dc.subject.MESH | Polycomb Repressive Complex 1 | - |
dc.subject.MESH | Proto-Oncogene Proteins/analysis | - |
dc.subject.MESH | Proto-Oncogene Proteins/physiology | - |
dc.subject.MESH | Proto-Oncogene Proteins p21(ras)/genetics | - |
dc.subject.MESH | Pulmonary Surfactant-Associated Protein B/analysis | - |
dc.subject.MESH | Repressor Proteins/analysis | - |
dc.subject.MESH | Repressor Proteins/physiology | - |
dc.subject.MESH | Urethane/toxicity | - |
dc.subject.MESH | Uteroglobin/analysis | - |
dc.title | Runx3 is required for the differentiation of lung epithelial cells and suppression of lung cancer. | - |
dc.type | Article | - |
dc.contributor.college | College of Dentistry (치과대학) | - |
dc.contributor.department | Dept. of Oral Biology (구강생물학) | - |
dc.contributor.googleauthor | K-S Lee | - |
dc.contributor.googleauthor | Y-S Lee | - |
dc.contributor.googleauthor | J-M Lee | - |
dc.contributor.googleauthor | K Ito | - |
dc.contributor.googleauthor | S Cinghu | - |
dc.contributor.googleauthor | J-H Kim | - |
dc.contributor.googleauthor | J-W Jang | - |
dc.contributor.googleauthor | Y-H Li | - |
dc.contributor.googleauthor | Y-M Goh | - |
dc.contributor.googleauthor | X-Z Chi | - |
dc.contributor.googleauthor | H Wee | - |
dc.contributor.googleauthor | H-W Lee | - |
dc.contributor.googleauthor | A Hosoya | - |
dc.contributor.googleauthor | J-H Chung | - |
dc.contributor.googleauthor | J-J Jang | - |
dc.contributor.googleauthor | J K Kundu | - |
dc.contributor.googleauthor | Y-J Surh | - |
dc.contributor.googleauthor | W-J Kim | - |
dc.contributor.googleauthor | Y Ito | - |
dc.contributor.googleauthor | H-S Jung | - |
dc.contributor.googleauthor | S-C Bae | - |
dc.identifier.doi | 10.1038/onc.2010.79 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A03758 | - |
dc.contributor.localId | A04640 | - |
dc.relation.journalcode | J02413 | - |
dc.identifier.eissn | 1476-5594 | - |
dc.identifier.pmid | 20228843 | - |
dc.identifier.url | http://www.nature.com/onc/journal/v29/n23/full/onc201079a.html | - |
dc.contributor.alternativeName | Lee, Jong Min | - |
dc.contributor.alternativeName | Jung, Han Sung | - |
dc.contributor.affiliatedAuthor | Jung, Han Sung | - |
dc.contributor.affiliatedAuthor | Lee, Jong Min | - |
dc.citation.volume | 29 | - |
dc.citation.number | 23 | - |
dc.citation.startPage | 3349 | - |
dc.citation.endPage | 3361 | - |
dc.identifier.bibliographicCitation | ONCOGENE, Vol.29(23) : 3349-3361, 2010 | - |
dc.identifier.rimsid | 52135 | - |
dc.type.rims | ART | - |
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