GPX3 suppresses tumor migration and invasion via the FAK/AKT pathway in esophageal squamous cell carcinoma

被引:5
作者
Zhu, Xiongjie [1 ]
Wang, Jiale [1 ]
Li, Lihua [1 ]
Deng, Lian [1 ]
Wang, Jinting [1 ]
Liu, Lu [1 ]
Zeng, Rong [1 ]
Wang, Qien [2 ]
Zheng, Yanfang [1 ]
机构
[1] Southern Med Univ, Dept Oncol, Zhujiang Hosp, Guangzhou 510282, Guangdong, Peoples R China
[2] Ohio State Univ, Wexner Med Ctr, Div Radiobiol, Dept Radiol, Columbus, OH 43210 USA
来源
AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH | 2018年 / 10卷 / 06期
关键词
Esophageal squamous cell carcinoma; glutathione peroxidase 3; FAK/AKT pathway; methylation; migration; invasion; GLUTATHIONE-PEROXIDASE; 3; HEPATOCELLULAR-CARCINOMA; CLINICAL-SIGNIFICANCE; DNA-DAMAGE; CANCER; EXPRESSION; TUMORIGENESIS; METHYLATION; GROWTH; MATRIX-METALLOPROTEINASE-9;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Although an increasing number of findings have proven that glutathione peroxidase 3 (GPX3) is methylated and down-regulated in various cancers, the underlying mechanism of its occurrence in esophageal squamous cell carcinoma (ESCC) remains unknown. In the present study, we found that the methylation rate in advanced cancers was significantly higher than that in early stage cancers by a methylation-specific polymerase chain reaction. Furthermore, the proliferation and migration capacities of KYSE-510 cells were inhibited after up-regulating GPX3 expression by GPX3 lentivirus transfection. As expected, the proliferation and migration capacities of KYSE-150 cells were promoted after down-regulating GPX3 expression with siRNA interfering. Moreover, we found that GPX3 might have deactivated the FAK/AKT signaling pathway to lower the expression of MMP-9 to suppress the migration and invasive capacities of KYSE-150 and KYSE-510 cells. Our findings suggested that GPX3 played a pivotal role in the suppression of carcinogenesis and progression in ESCC, and GPX3 has the potential as a novel biomarker in the diagnosis of ESCC.
引用
收藏
页码:1908 / 1920
页数:13
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