STAT5A-mediated NOX5-L expression promotes the proliferation and metastasis of breast cancer cells

被引:27
作者
Dho, So Hee [1 ,2 ]
Kim, Ji Young [1 ]
Lee, Kwang-Pyo [1 ]
Kwon, Eun-Soo [1 ]
Lim, Jae Cheong [2 ]
Kim, Chang-Jin [3 ]
Jeong, Dongjun [3 ]
Kwon, Ki-Sun [1 ,4 ]
机构
[1] Korea Res Inst Biosci & Biotechnol, Aging Res Ctr, Daejeon 305806, South Korea
[2] Korea Atom Energy Res Inst, Dept Res Reactor Utilizat, Radioisotope Res Div, Taejon 305353, South Korea
[3] Soonchunhyang Med Sci Res Inst, Dept Pathol, Cheonan 330090, South Korea
[4] Korea Univ Sci & Technol UST, Dept Funct Genom, Daejeon 305333, South Korea
基金
新加坡国家研究基金会;
关键词
Cancer; NOX5-L; ROS; STAT5A; ESOPHAGEAL ADENOCARCINOMA CELLS; NADPH OXIDASE NOX5-S; PROSTATE-CANCER; OXIDATIVE STRESS; ACTIVATION; MECHANISM; APOPTOSIS; NOX1; GENES; RAS;
D O I
10.1016/j.yexcr.2016.12.020
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
NADPH oxidase (NOX) generates reactive oxygen species (ROS) and has been suggested to mediate cell proliferation in some cancers. Here, we show that an increase in the expression of NOX5 long form (NOX5-L) is critical for tumor progression in breast tumor tissues. Immunostaining of clinical samples indicated that NOX5 was overexpressed in 41.1% of breast ductal carcinoma samples. NOX5-L depletion consistently suppressed cell proliferation, invasion, and migration in vitro. Antibody-mediated neutralization of NOX5-L attenuated tumor progression in a mouse xenograft model. Promoter analysis revealed that NOX5-L expression is regulated by STAT5A in breast cancer cells. Based on our novel findings, we suggest that inhibition of NOX5-L may be a promising therapeutic strategy that exerts anti-cancer effects via the modulation of ROS-mediated cell signaling.
引用
收藏
页码:51 / 58
页数:8
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