کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3164671 | 1198804 | 2011 | 8 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: The involvement of CHD5 hypermethylation in laryngeal squamous cell carcinoma The involvement of CHD5 hypermethylation in laryngeal squamous cell carcinoma](/preview/png/3164671.png)
SummaryChromodomain 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.
Journal: Oral Oncology - Volume 47, Issue 7, July 2011, Pages 601–608