depletion of hdac6 enhances cisplatin-induced dna damage and apoptosis in non-small cell lung cancer cells损耗的hdac6增强cisplatin-induced dna损伤,在非小细胞肺癌细胞凋亡.pdfVIP
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depletion of hdac6 enhances cisplatin-induced dna damage and apoptosis in non-small cell lung cancer cells损耗的hdac6增强cisplatin-induced dna损伤,在非小细胞肺癌细胞凋亡
Depletion of HDAC6 Enhances Cisplatin-Induced DNA Damage and Apoptosis in Non-Small Cell Lung Cancer Cells 1. 1. 1 1 1,2 1,3 Lei Wang , Shengyan Xiang , Kendra A. Williams , Huiqin Dong , Wenlong Bai , Santo V. Nicosia , 4 5 1,2 Saadi Khochbin , Gerold Bepler *, Xiaohong Zhang * 1 Department of Pathology and Cell Biology, University of South Florida, Morsani College of Medicine, Tampa, Florida, United States of America, 2 Program of Molecular Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida, United States of America, 3 Experimental Therapeutics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida, United States of America, 4 French National Institute of Health and Medical Research, The Albert Bonniot Institute, Grenoble, France, 5 Department of Oncology, Karmanos Cancer Institute, Detroit, Michigan, United States of America Abstract Histone deacetylase inhibitors (HDACi) are promising therapeutic agents which are currently used in combination with chemotherapeutic agents in clinical trials for cancer treatment including non-small cell lung cancer (NSCLC). However, the mechanisms underlying their anti-tumor activities remain elusive. Previous studies showed that inhibition of HDAC6 induces DNA damage and sensitizes transformed cells to anti-tumor agents such as etoposide and doxorubicin. Here, we showed that depletion of HDAC6 in two NSCLC cell lines, H292 and A549, sensitized cells to cisplatin, one of the first-line chemotherapeutic agents used to treat NSCLC. We suggested
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