DNA methylation directly downregulates human cathelicidin antimicrobial peptide gene (CAMP) promoter activity
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Xi Chen1,*, Guangying Qi2,4,*, Mingqun Qin3,*, Yantao Zou1, Kanghua Zhong1, Ying Tang1, Yong Guo1, Xinxiang Jiang3, Lihua Liang3, Xianqiong Zou1
1College of Biotechnology, Guilin Medical University, Guilin 541100, Guangxi, P. R. China
2Department of Pathology and Physiopathology, Guilin Medical University, Guilin 541004, Guangxi, P. R. China
3Department of Stomatology, Affiliated Hospital of Guilin Medical University, Guilin 541004, Guangxi, P. R. China
4Laboratory of Tumor Immunology and Microenvironmental Regulation, Guilin Medical University, Guilin 541004, Guangxi, P. R. China
*These authors contributed equally to this work
Xianqiong Zou, email: email@example.com
Keywords: CAMP, LL-37, OSCC, DNA methylation, promoter
Received: September 01, 2016 Accepted: February 20, 2017 Published: March 02, 2017
LL-37, the active product of human cathelicidin antimicrobial peptide (CAMP) has a broad spectrum of antibacterial activity. LL-37 also has important physiological functions in immune regulation, angiogenesis and in modulating apoptosis. The roles of LL-37 in oral squamous cell carcinoma (OSCC) are still not clear. The correlation between DNA methylation and human CAMP expression is also unknown. Here human CAMP/LL-37 expression was assessed by immunohistochemistry in normal and OSCC tissues. The results indicated that low expression of CAMP/LL-37 correlated with histological differentiation and lymph node metastasis and also promoted tumor progression. A cell-specific methylation pattern in the promoter region of human CAMP was detected. Treatment with 5-aza-2’-deoxycytidine, a DNA demethylation reagent can increase human CAMP expression in epithelial cancer cells. The reporter assay showed that unmethylated human CAMP promoter activity was significantly higher than methylated promoter activity. Taken together, these results suggested that human CAMP/LL-37 might act as a tumor-suppressor in OSCC and DNA methylation might play roles during carcinogenesis via directly downregulating human CAMP promoter activity.
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