期刊
JOURNAL OF ONCOLOGY
卷 2011, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2011/609259
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- National Science Council [NSC-97-3111-B-075-001-MY3/98-2314-B-075-008-MY3]
- Taipei Veterans General Hospital [V97B1-006/E1-008/F-001/F-010]
- National Yang-Ming University ( Ministry of Education, Aim for the Top University Plan)
- Chung Shan Medical University Hospital [CSH-2010-C-025]
- Technology Development Program for Academia [98-EC-17-A-19-S2-0107]
- Department of Industrial Technology, Ministry of Economic Affairs, Taiwan
Recent studies suggest that ALDH1 is a putative marker for HNSCC-derived cancer stemcells. However, the regulation mechanisms that maintain the stemness and metastatic capability of HNSCC-ALDH1(+) cells remain unclear. Initially, HNSCC-ALDH1(+) cells from HNSCC patient showed cancer stemness properties, and high expression of Bmi1 and Snail. Functionally, tumorigenic properties of HNSCC-ALDH1(+) cells could be downregulated by knockdown of Bmi-1. Overexpression of Bmi-1 altered in expression property ALDH1-cells to that of ALDH1(+) cells. Furthermore, knockdown of Bmi-1 enhanced the radiosensitivity of radiation-treated HNSCC-ALDH1(+) cells. Moreover, overexpression of Bmi-1 in HNSCC-ALDH1-cells increased tumor volume and number of pulmonary metastatic lesions by xenotransplant assay. Importantly, knock-down of Bmi1 in HNSCC-ALDH1(+) cells significantly decreased distant metastases in the lungs. Clinically, coexpression of Bmi-1/Snail/ALDH1 predicted the worst prognosis in HNSCC patients. Collectively, our data suggested that Bmi-1 plays a key role in regulating Snail expression and cancer stemness properties of HNSCC-ALDH1(+) cells.
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