Effect of Trichostatin A on CNE2 Nasopharyngeal Carcinoma Cells - Genome-wide DNA Methylation Alteration
Autor: | Xing Lina, Xiao-Chun Liu, Xiaoli Yang, Yong-Hu Wu, Shao-Ming Lu, Hua Wu, Huayu Wu, Meng-Bin Qin, Cheng-Dong Zhang, Zhang Yuening |
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Rok vydání: | 2014 |
Předmět: |
Cancer Research
Epidemiology Apoptosis Hydroxamic Acids Cell Line Tumor medicine Humans Cell Proliferation Nasopharyngeal Carcinoma biology Cell growth Carcinoma Cell Cycle Public Health Environmental and Occupational Health Nasopharyngeal Neoplasms Methylation DNA Methylation Molecular biology Histone Trichostatin A Oncology Acetylation DNA methylation biology.protein Cancer research Histone deacetylase Genome-Wide Association Study medicine.drug |
Zdroj: | Asian Pacific Journal of Cancer Prevention. 15:4663-4670 |
ISSN: | 1513-7368 |
Popis: | Trichostatin A (TSA) is a histone deacetylase (HDAC) inhibitor. We here investigated its effects on proliferation and apoptosis of the CNE2 carcinoma cell line, and attempted to establish genome-wide DNA methylation alteration due to differentially histone acetylation status. After cells were treated by TSA, the inhibitory rate of cell proliferation was examined with a CCK8 kit, and cell apoptosis was determined by flow cytometry. Compared to control, TSA inhibited CNE2 cell growth and induced apoptosis. Furthermore, TSA was found to induce genome-wide methylation alteration as assessed by genome-wide methylation array. Overall DNA methylation level of cells treated with TSA was higher than in controls. Function and pathway analysis revealed that many genes with methylation alteration were involved in key biological roles, such as apoptosis and cell proliferation. Three genes (DAP3, HSPB1 and CLDN) were independently confirmed by quantitative real-time PCR. Finally, we conclude that TSA inhibits CNE2 cell growth and induces apoptosis in vitro involving genome-wide DNA methylation alteration, so that it has promising application prospects in treatment of NPC in vivo. Although many unreported hypermethylated/hypomethylated genes should be further analyzed and validated, the pointers to new biomarkers and therapeutic strategies in the treatment of NPC should be stressed. |
Databáze: | OpenAIRE |
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