FGF2 regulates proliferation, migration, and invasion of ECA109 cells through PI3K/Akt signalling pathway in vitro. (9th March 2016)

• Record Type: Journal Article
• Authors: Shi, Hui; Xu, Jingjing; Zhao, Rui; Wu, Huiqun; Gu, Luo; Chen, Yijiang
• Is Part Of: Cell biology international. Volume 40:Number 5(2016)
• Page Start: 524
• Page End: 533
• Publication Date: 2016-03-09
• Subjects: ECA109 -- esophageal cancer -- FGF2 -- invasion -- migration -- PI3K/Akt signalling pathway; Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.10588
• Languages: English
• ISSNs: 1065-6995

Abstract

Abstract: Esophageal cancer is one of the most common malignant cancers that arise from esophagus tissues. Fibroblast growth factor 2 (FGF2) has been implicated in multiple biological functions and was considered as an oncogenic factor in tumorigenesis. However, the effects of FGF2 in esophageal carcinoma are yet to be fully elucidated. To better understand the function of FGF2 in esophageal cancer, we used the esophageal cancer cell line ECA109 as a cell model and downregulated FGF2 expression using RNAi; the results showed that insufficient expression of FGF2 inhibited cells proliferation, migration, and invasion of ECA109 cells. Meanwhile, the proliferation, migration, and invasion abilities were stimulated after treatment of exogenous FGF2. In addition, a PI3K/Akt signalling pathway inhibitor (LY294002) alleviated the tumorigenic effects of FGF2. These findings implied that the oncogenic effects of FGF2 was mediated, at least in part, through the PI3K/Akt signalling pathway and FGF2 may be a potential therapeutic target to constrain the tumorigenesis of esophageal cancer.