期刊
ONCOGENE
卷 29, 期 44, 页码 5969-5975出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2010.330
关键词
EMX2; methylation; lung cancer; WNT signaling; tumor suppression
资金
- Joan's Legacy: uniting against Lung Cancer Research Grant
- NIH/NCI [R01CA125030, R01CA130980, R01CA13256]
- Eileen D Ludwig endowed for Thoracic Oncology Research
- Bonnie J Addario Lung Cancer Foundation
- Kazan foundation
- McClain foundation
- Abrams foundation
- Fernandez foundation
- Lyons foundation
- Greenwood foundation
- Harley and Oberman Foundation
- Barbara Isackson Lung Cancer Research Fund
- Swedish Cancer Institute
- DOD [W81XWH-06-1-0416]
Lung cancer is a common cancer and the leading cause of cancer-related death worldwide. Aberrant activation of WNT signaling is implicated in lung carcinogenesis. EMX2, a human homologue of the Drosophila empty spiracles gene is a homeodomain-containing transcription factor. The function of EMX2 has been linked to the WNT signaling pathway during embryonic patterning in mice. However, little is known about the role of EMX2 in human tumorigenesis. In this study, we found that EMX2 was dramatically downregulated in lung cancer tissue samples and this downregulation was associated with methylation of the EMX2 promoter. Restoration of EMX2 expression in lung cancer cells lacking endogenous EMX2 expression suppressed cell proliferation and invasive phenotypes, inhibited canonical WNT signaling, and sensitized lung cancer cells to the treatment of the chemo cytotoxic drug cisplatin. On the other hand, knockdown of EMX2 expression in lung cancer cells expressing endogenous EMX2 promoted cell proliferation, invasive phenotypes and canonical WNT signaling. Taken together, our study suggests that EMX2 may have important roles as a novel suppressor in human lung cancer. Oncogene (2010) 29, 5969-5975; doi:10.1038/onc.2010.330; published online 9 August 2010
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