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Báo cáo y học: "Histone deacetylases (HDACs) in XPC gene silencing and bladder cancer"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Histone deacetylases (HDACs) in XPC gene silencing and bladder cancer. | Xu et al. Journal of Hematology Oncology 2011 4 17 http www.jhoonline.Org content 4 1 17 JOURNAL OF HEMATOLOGY ONCOLOGY RESEARCH Open Access Histone deacetylases HDACs in XPC gene silencing and bladder cancer Xiaoxin S Xu1 Le Wang1 Judith Abrams2 and Gan Wang1 Abstract Bladder cancer is one of the most common malignancies and causes hundreds of thousands of deaths worldwide each year. Bladder cancer is strongly associated with exposure to environmental carcinogens. It is believed that DNA damage generated by environmental carcinogens and their metabolites causes development of bladder cancer. Nucleotide excision repair NER is the major DNA repair pathway for repairing bulk DNA damage generated by most environmental carcinogens and XPC is a DNA damage recognition protein required for initiation of the NER process. Recent studies demonstrate reduced levels of XPC protein in tumors for a majority of bladder cancer patients. In this work we investigated the role of histone deacetylases HDACs in XPC gene silencing and bladder cancer development. The results of our HDAC inhibition study revealed that the treatment of HTB4 and HTB9 bladder cancer cells with the HDAC inhibitor valproic acid VPA caused an increase in transcription of the XPC gene in these cells. The results of our chromatin immunoprecipitation ChIP studies indicated that the VPA treatment caused increased binding of both CREB1 and Sp1 transcription factors at the promoter region of the XPC gene for both HTB4 and HTB9 cells. The results of our immunohistochemistry IHC staining studies further revealed a strong correlation between the over-expression of HDAC4 and increased bladder cancer occurrence p 0.001 as well as a marginal significance of increasing incidence of HDAC4 positivity seen with an increase in severity of bladder cancer p 0.08 . In addition the results of our caspase 3 activation studies demonstrated that prior treatment with VPA increased the anticancer drug cisplatin-induced activation of .