Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/40145
標題: Overexpression of optic atrophy 1 protein increases cisplatin resistance via inactivation of caspase-dependent apoptosis in lung adenocarcinoma cells
作者: Fang, Hsin-Yuan
Chen, Chih-Yi
Chiou, Shiow-Her
Wang, Yu-Ting
Lin, Tze-Yi
Chang, Hui-Wen
Chiang, I-Ping
Lan, Kuo-Jung
Chow, Kuan-Chih
關鍵字: Apoptosis-inducing factor;Caspase;Cytochrome c;Drug resistance;Mitochondrial membrane;mitochondrial fusion;cytochrome-c;cigarette-smoking;cancer cells;opa1;fission;release;expression;life
Project: Human Pathology, Volume 43, Issue 1, Page(s) 105-114.
摘要: 
Optic atrophy 1 protein, a 112-kd guanosine triphosphatase, is involved in the mitochondrial inner membrane fusion and anticancer drug-mediated cytotoxicity, which implicate an association with disease progression of the cancer. In this study, we investigated the prognostic value of optic atrophy 1 expression in patients with lung adenocarcinoma. Using immunohistochemical staining, expression of optic atrophy 1 was determined in 286 lung adenocarcinoma patients. Expression of optic atrophy 1 was confirmed by immunoblotting. The relationship between optic atrophy 1 expression and clinicopathological parameters was analyzed statistically by comparing survival between different groups using the log-rank test. The results showed that optic atrophy 1 overexpression was detected in 219 (76.6%) of lung adenocarcinoma patients. A significant difference was found in cumulative survival between patients with high optic atrophy 1 levels and those with low optic atrophy 1 levels (P = .0016). In the in vitro experiments with cell lines, silencing of optic atrophy 1 expression reduced cisplatin resistance, which was further shown via increased release of cytochrome c and activation of caspase-dependent apoptotic pathway. In conclusion, optic atrophy 1 is highly expressed in lung adenocarcinoma and indicates poor prognosis. (C) 2012 Elsevier Inc. All rights reserved.
URI: http://hdl.handle.net/11455/40145
ISSN: 0046-8177
DOI: 10.1016/j.humpath.2011.04.012
Appears in Collections:生物醫學研究所

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