The Journal of international medical research · 2020
NLRC5 promotes cell migration and invasion by activating the PI3K/AKT signaling pathway in endometrial cancer.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Fan Yijun, Dong Zhen, Shi Yuchuan, Sun Shiying, Wei Bing, Zhan Lei
Аннотация
OBJECTIVE: NOD-like receptor family caspase recruitment domain family domain-containing 5 (NLRC5) is involved in the development of cancer. Our objective was to explore the role of NLRC5 in the progression of endometrial cancer (EC).
METHODS: The roles of NLRC5 in migration and invasion of AN3CA EC cells were examined by cell wound-healing assay, Transwell migration, and invasion analysis. Overexpression of NLRC5 was achieved with NLRC5 plasmid, and knockdown of NLRC5 was achieved using small interfering (si)RNA-NLRC5 in AN3CA cells. The expression of NLRC5 was detected by immunohistochemical, western blot, and quantitative real-time PCR. LY294002 was used to inhibit the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway.
RESULTS: NLRC5 was downregulated in EC tissue compared with normal endometrium. Overexpression of NLRC5 led to upregulation of cell migration and invasion in AN3CA cells and expression of matrix metallopeptidase (MMP)-9. Inhibition of NLRC5 restricted migration and invasion of AN3CA cells and expression of MMP9. Overexpression of NLRC5 promoted the activation of PI3K/AKT signaling pathway. Inhibiting PI3K/AKT signaling pathway by using LY294002 blocked the positive role of NLRC5 in migration and invasion of AN3CA cells and expression of MMP9.
CONCLUSIONS: These results demonstrate that NLRC5 promotes EC progression by activating the PI3K/AKT signaling pathway.
METHODS: The roles of NLRC5 in migration and invasion of AN3CA EC cells were examined by cell wound-healing assay, Transwell migration, and invasion analysis. Overexpression of NLRC5 was achieved with NLRC5 plasmid, and knockdown of NLRC5 was achieved using small interfering (si)RNA-NLRC5 in AN3CA cells. The expression of NLRC5 was detected by immunohistochemical, western blot, and quantitative real-time PCR. LY294002 was used to inhibit the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway.
RESULTS: NLRC5 was downregulated in EC tissue compared with normal endometrium. Overexpression of NLRC5 led to upregulation of cell migration and invasion in AN3CA cells and expression of matrix metallopeptidase (MMP)-9. Inhibition of NLRC5 restricted migration and invasion of AN3CA cells and expression of MMP9. Overexpression of NLRC5 promoted the activation of PI3K/AKT signaling pathway. Inhibiting PI3K/AKT signaling pathway by using LY294002 blocked the positive role of NLRC5 in migration and invasion of AN3CA cells and expression of MMP9.
CONCLUSIONS: These results demonstrate that NLRC5 promotes EC progression by activating the PI3K/AKT signaling pathway.
Предметные рубрики MeSH
Cell Line, TumorCell MovementCell ProliferationChromonesDisease ProgressionEndometrial NeoplasmsEndometriumFemaleHumansHysterectomyIntracellular Signaling Peptides and ProteinsMatrix Metalloproteinase 9Middle AgedMorpholinesNeoplasm InvasivenessPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktSignal Transduction