| Literature DB >> 30018730 |
Xiongjie Zhu1, Jiale Wang1, Lihua Li1, Lian Deng1, Jinting Wang1, Lu Liu1, Rong Zeng1, Qien Wang2, Yanfang Zheng1.
Abstract
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.Entities:
Keywords: Esophageal squamous cell carcinoma; FAK/AKT pathway; glutathione peroxidase 3; invasion; methylation; migration
Year: 2018 PMID: 30018730 PMCID: PMC6038073
Source DB: PubMed Journal: Am J Transl Res Impact factor: 4.060