Lin Ye1, Tingxiu Xiang1, Yu Fan2, Dongsheng Zhang3,4, Lili Li3, Chong Zhang1, Xiaoqian He1, Qin Xiang1, Qian Tao1,3, Guosheng Ren1. 1. Chongqing Key Laboratory of Molecular Oncology & Epigenetics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, PR China. 2. Department of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, PR China. 3. Cancer Epigenetics Laboratory, Department of Clinical Oncology, Sir YK Pao Center for Cancer & Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong & CUHK-Shenzhen Research Institute, Hong Kong, PR China. 4. Department of Medical Oncology, Sun Yat-sen University Cancer Center, Guangzhou 510060, PR China.
Abstract
AIM: To study the epigenetic alternations and biological functions of ZFP82 in esophageal squamous cell carcinoma. MATERIALS & METHODS: Analysis of ZFP82 expression was carried out by quantitative real-time PCR. Cell function was tested by MTS cell proliferation assay, transwell assay and flow cytometry. Gene mechanisms were studied by reverse transcription-PCR (RT-PCR), quantitative real-time PCR, luciferase reporter assay and Western blot. RESULTS: ZFP82 promoter methylation was downregulated in esophageal squamous cell carcinoma. ZFP82 ectopic expression suppressed cell function and regulated NF-κB phosphorylation and genes involved in cell cycle arrest and apoptosis. Moreover, ZFP82 methylation was correlated with age, tumor stage and outcome. CONCLUSION: ZFP82 is a tumor suppressor and is disrupted by promoter CpG methylation during esophageal carcinogenesis.
AIM: To study the epigenetic alternations and biological functions of ZFP82 in esophageal squamous cell carcinoma. MATERIALS & METHODS: Analysis of ZFP82 expression was carried out by quantitative real-time PCR. Cell function was tested by MTS cell proliferation assay, transwell assay and flow cytometry. Gene mechanisms were studied by reverse transcription-PCR (RT-PCR), quantitative real-time PCR, luciferase reporter assay and Western blot. RESULTS:ZFP82 promoter methylation was downregulated in esophageal squamous cell carcinoma. ZFP82 ectopic expression suppressed cell function and regulated NF-κB phosphorylation and genes involved in cell cycle arrest and apoptosis. Moreover, ZFP82 methylation was correlated with age, tumor stage and outcome. CONCLUSION:ZFP82 is a tumor suppressor and is disrupted by promoter CpG methylation during esophageal carcinogenesis.