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Overexpression of PLK1 is associated with poor survival by inhibiting apoptosis via enhancement of survivin level in esophageal squamous cell carcinoma
Author(s) -
Feng YanBin,
Lin DeChen,
Shi ZhiZhou,
Wang XiaoChun,
Shen XiaoMing,
Zhang Yu,
Du XiaoLi,
Luo ManLi,
Xu Xin,
Han YaLing,
Cai Yan,
Zhang ZiQiang,
Zhan QiMin,
Wang MingRong
Publication year - 2008
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.23990
Subject(s) - survivin , plk1 , downregulation and upregulation , cancer research , apoptosis , biology , cell cycle , gene , biochemistry
PLK1 is essential for the maintenance of genomic stability during mitosis. In our study, we found that overexpression of PLK1 was an independent prognostic factor (RR = 4.253, p = 0.020) and significantly correlated with survivin, an antiapoptotic protein, in esophageal squamous cell carcinoma (ESCC). Reverse transcription‐polymerase chain reaction and fluorescence in situ hybridization (FISH) revealed upregulation of PLK1 mRNA and amplification of PLK1 gene, respectively. Depletion of PLK1 activated the intrinsic apoptotic pathway, which was substantiated by loss of mitochondrial membrane potential, reduction of Mcl‐1 and Bcl‐2 as well as activation of caspase‐9. Coimmunoprecipitation and confocal microscopy displayed that PLK1 was associated with survivin and PLK1 depletion led to downregulation of survivin. Cotransfection of survivin constructs could partially reverse PLK1‐depletion‐induced apoptosis. These data suggest that PLK1 might be a useful prognostic marker and a potential therapeutic target for ESCC. Survivin is probably involved in antiapoptotic function of PLK1. © 2008 Wiley‐Liss, Inc.