1. EFNB2 facilitates cell proliferation, migration, and invasion in pancreatic ductal adenocarcinoma via the p53/p21 pathway and EMT.
- Author
-
Zhu F, Dai SN, Xu DL, Hou CQ, Liu TT, Chen QY, Wu JL, and Miao Y
- Subjects
- Adenocarcinoma genetics, Carcinoma, Pancreatic Ductal genetics, Cell Movement, Cell Proliferation, Ephrin-B2 genetics, Gene Expression Regulation, Neoplastic, Humans, Tumor Suppressor Protein p53 genetics, p21-Activated Kinases genetics, Adenocarcinoma metabolism, Carcinoma, Pancreatic Ductal metabolism, Ephrin-B2 metabolism, Tumor Suppressor Protein p53 metabolism, p21-Activated Kinases metabolism
- Abstract
Ephrin-2 (EFNB2) is expressed at abnormally high levels in some neoplasms, such as squamous cell carcinoma of the head and neck and colorectal cancer. Its overexpression is associated with the malignant progression of tumors. However, the expression of EFNB2 in pancreatic ductal adenocarcinoma (PDAC) has not been thoroughly studied. EFNB2 expression was evaluated by quantitative real-time PCR, immunohistochemistry, and western blotting. Furthermore, the association between its expression levels and the clinicopathological features of PDAC patients was explored. To determine the underlying mechanisms of EFNB2, we transfected PDAC cells with small interfering RNA and performed in vitro and in vivo experiments. EFNB2 expression levels were significantly increased in cancer tissues and were associated with PDAC clinical stage and Ki67 expression. The down-regulation of EFNB2 inhibited cell proliferation by up-regulating p53/p21-mediated G0/G1 phase blockade. Knockdown of EFNB2 decreased the migration and invasion of PDAC cells by blocking epithelial-mesenchymal transition. These results suggested that EFNB2 may participate in the development of PDAC by promoting cell proliferation, migration, and invasion. Thus, EFNB2 is a potential target for the diagnosis and treatment of PDAC., Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest., (Copyright © 2020 The Author(s). Published by Elsevier Masson SAS.. All rights reserved.)
- Published
- 2020
- Full Text
- View/download PDF