Dual-specificity Phosphatase 1 Deficiency Induces Endometrioid Adenocarcinoma Progression via Activa

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Background:Previously,we reported that dual-specificity phosphatase 1 (DUSP1) was differentially expressed in endometrioid adenocarcinoma (EEA).However,the role of DUSP1 in EEA progression and the relationship between DUSP1 and medroxyprogesterone (MPA) are still unclear.Methods:The expression of DUSP 1 in EEA specimens was detected by immunohistochemical analysis.The effect of DUSP 1 on cell proliferation was analyzed by Cell Counting Kit 8 and colony formation assay,and cell migration was analyzed by transwell assay.MPA-induced DUSP1 expression in EEA cells was measured by West blot.Results:DUSP1 expression was deficient in advanced Intational Federation of Gynecology and Obstetrics stage,high-grade and myometrial invasive EEA.In EEA cell lines (HeclA,HeclB,RL952,and Ishikawa),the DUSP1 expression was substantially higher in Ishikawa cells than in other cell lines (P < 0.05).Knockdown of DUSP1 promoted Ishikawa cells proliferation,migration,and activation of mitogen-activated protein kinases/extracellular signal-regulated kinase (MAPK/Erk) pathway.MPA-induced DUSP1 expression and inhibited MAPK/Erk pathway in Ishikawa cells.Conclusions:Our data suggest that DUSP1 deficiency promotes EEA progression via MAPK/Erk pathway,which may be reversed by MPA,suggesting that DUSP 1 may serve as a potential therapeutic target for the treatment of EEA.
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