Dual-specificity Phosphatase 1 Deficiency Induces Endometrioid Adenocarcinoma Progression via Activation of Mitogen-activated Protein Kinase/Extracellular Signal-regulated Kinase Pathway

• Published in: Chinese medical journal 2016-05, Vol.129 (10), p.1154-1160
• Main Authors: Yang, Yuan, Zhou, Jing-Yi, Zhao, Li-Jun, Gao, Bao-Rong, Wan, Xiao-Ping, Wang, Jian-Liu
• Format: Article
• Language: English
• Subjects: Breast cancer; Carcinoma, Endometrioid - metabolism; Cell Culture Techniques; Cell growth; Cell Proliferation - genetics; Cell Proliferation - physiology; Dual-specificity Phosphatase 1; Endometrioid Adenocarcinoma; Medroxyprogesterone; Phospho-extracellular Signal-regulated Kinase 1/2; Dual-Specificity Phosphatases - genetics; Dual-Specificity Phosphatases - metabolism; Endometrial cancer; Experiments; Extracellular Signal-Regulated MAP Kinases - metabolism; Female; Gene expression; Gynecology; Humans; Kinases; Liver cancer; Lung cancer; Mitogen-Activated Protein Kinases - metabolism; Obstetrics; Original; Penicillin; Phosphatase; Prostate cancer; Proteins; 丝裂原活化蛋白激酶; 信号通路; 子宫内膜; 异性; 激活; 磷酸酶; 细胞外信号调节激酶; 腺癌
• ISSN: 0366-6999; 2542-5641
• DOI: 10.4103/0366-6999.181954

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.