Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/69037
標題: Overexpression of optic atrophy 1 protein increases cisplatin resistance via inactivation of caspase-dependent apoptosis in lung adenocarcinoma cells
作者: Fang, H.Y.
Chen, C.Y.
Chiou, S.H.
Wang, Y.T.
Lin, T.Y.
Chang, H.W.
Chiang, I.P.
Lan, K.J.
Chow, K.C.
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
期刊/報告no:: 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/11455/69037
ISSN: 0046-8177
文章連結: http://dx.doi.org/10.1016/j.humpath.2011.04.012
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