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.