Asset Details
Do you wish to reserve the book?
Dual-specificity Phosphatase 1 Deficiency Induces Endometrioid Adenocarcinoma Progression via Activation of Mitogen-activated Protein Kinase/Extracellular Signal-regulated Kinase Pathway
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Dual-specificity Phosphatase 1 Deficiency Induces Endometrioid Adenocarcinoma Progression via Activation of Mitogen-activated Protein Kinase/Extracellular Signal-regulated Kinase Pathway
Do you wish to request the book?
Dual-specificity Phosphatase 1 Deficiency Induces Endometrioid Adenocarcinoma Progression via Activation of Mitogen-activated Protein Kinase/Extracellular Signal-regulated Kinase Pathway
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Dual-specificity Phosphatase 1 Deficiency Induces Endometrioid Adenocarcinoma Progression via Activation of Mitogen-activated Protein Kinase/Extracellular Signal-regulated Kinase Pathway
2016
Overview
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.
Publisher
Wolters Kluwer - Medknow Publications,Lippincott Williams & Wilkins Ovid Technologies,Department of Obstetrics and Gynecology,Peking University People's Hospital,Beijing 100044,China%Department of Obstetrics and Gynecology,West China Second University Hospital,Sichuan University,Chengdu,Sichuan 610041,China%Department of Gynecology,Tongji University School of Medicine Affiliated Shanghai First Maternity and Infant Hospital,Shanghai 200126,China,Medknow Publications & Media Pvt Ltd,Wolters Kluwer
Subject
/ Carcinoma, Endometrioid - metabolism
/ Cell Proliferation - genetics
/ Cell Proliferation - physiology
/ Dual-Specificity Phosphatases - genetics
/ Dual-Specificity Phosphatases - metabolism
/ Extracellular Signal-Regulated MAP Kinases - metabolism
/ Female
/ Humans
/ Kinases
/ Mitogen-Activated Protein Kinases - metabolism
/ Original
/ Proteins
/ 信号通路
/ 子宫内膜
/ 异性
/ 激活
/ 磷酸酶
/ 腺癌
