Background: Previously, we reported that dual-specificity adenocarcinoma (EEA). However, the role of DUSP1 medroxyprogesterone (MPA) are still unclear. phosphatase I (DUSPI) was differentially expressed in endo...Background: Previously, we reported that dual-specificity adenocarcinoma (EEA). However, the role of DUSP1 medroxyprogesterone (MPA) are still unclear. phosphatase I (DUSPI) was differentially expressed in endometrioid in EEA progression and the relationship between DUSPI and Methods: The expression of DUSPI in EEA specimens was detected by immunohistochemical analysis. The effect of DUSPI on cell proliferation was analyzed by Cell Counting Kit 8 and colony formation assay, and cell migration was analyzed by transwell assay. MPA-induced DUSPI expression in EEA cells was measured by Western blot. Results: DUSPI expression was deficient in advanced International Federation of Gynecology and Obstetrics stage, high-grade and myometrial invasive EEA. In EEA cell lines (HeclA, Hecl B, RL952, and Ishikawa), the DUSP1 expression was substantially higher in lshikawa cells than in other cell lines (P 〈 0.05). Knockdown ofDUSP I promoted lshikawa 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 I may serve as a potential therapeutic target for the treatment of EEA.展开更多
文摘Background: Previously, we reported that dual-specificity adenocarcinoma (EEA). However, the role of DUSP1 medroxyprogesterone (MPA) are still unclear. phosphatase I (DUSPI) was differentially expressed in endometrioid in EEA progression and the relationship between DUSPI and Methods: The expression of DUSPI in EEA specimens was detected by immunohistochemical analysis. The effect of DUSPI on cell proliferation was analyzed by Cell Counting Kit 8 and colony formation assay, and cell migration was analyzed by transwell assay. MPA-induced DUSPI expression in EEA cells was measured by Western blot. Results: DUSPI expression was deficient in advanced International Federation of Gynecology and Obstetrics stage, high-grade and myometrial invasive EEA. In EEA cell lines (HeclA, Hecl B, RL952, and Ishikawa), the DUSP1 expression was substantially higher in lshikawa cells than in other cell lines (P 〈 0.05). Knockdown ofDUSP I promoted lshikawa 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 I may serve as a potential therapeutic target for the treatment of EEA.