期刊
ORAL ONCOLOGY
卷 47, 期 7, 页码 601-608出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.oraloncology.2011.05.003
关键词
CHD5; Hypermethylation; Laryngeal squamous cell carcinoma; Immunohistochemistry; Sequencing; Apoptosis
资金
- National Nature Science Foundation of China [30700980]
- National 863 Project of China [2002BA711A08-18]
- Natural Science Foundation of Liaoning Province [20092110]
Chromodomain helicase DNA-binding protein 5 (CHD5) has been found to be a candidate tumor suppressor gene (TSG) in malignant neural tumors. In mice heterozygous for chd5 deficiency, the first tumor observed was pathological squamous cell carcinoma. More than 95% of primary laryngeal cancer is squamous cell carcinoma. Thus, we explored the expression of CHD5 in 65 patients with laryngeal squamous cell carcinoma (LSCC) using real-time PCR, immunohistochemistry and Western blotting. DNA methylation was detected using bisulfate-specific sequencing. The potential function of CHD5 was determined using MTT, apoptosis and transwell migration assays in CHD5-transfected Hep-2 cells. Our results revealed that the mRNA and protein expression levels of CHD5 in LSCC tissues were significantly lower than those in clear surgical margin tissues (p < 0.05), and there is a significant correlation between the mRNA and protein expression levels of CHD5 (p < 0.01). In addition, there were significant differences in CHD5 mRNA and protein levels with respect to the patient's clinical stage (p < 0.05). Aberrant methylation of the CHD5 promoter was frequently found in the Hep-2 cell line and LSCC tumor tissues, especially tumor tissues from advanced TNM (p < 0.05) or older patients (p < 0.05). Finally, ectopic expression of CHD5 in laryngeal cancer cells led to significant inhibition of growth and invasiveness. Our data suggest that CHD5 is a tumor suppressor gene that is epigenetically downregulated in LSCC. (C) 2011 Elsevier Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据