title: FGF2 regulates proliferation, migration, and invasion of ECA109 cells through PI3K/Akt signalling pathway in vitro.
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.
authors.affiliation: Department of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210000, Jiangsu, China.|Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, 210000, Jiangsu, China.|Department of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Shi
authors.affiliation: Nursing School of Nantong University, Nantong, 226001, Jiangsu, China.
authors.forename: Jingjing
authors.initials: J
authors.lastname: Xu
authors.affiliation: Nursing School of Nantong University, Nantong, 226001, Jiangsu, China.
authors.forename: Rui
authors.initials: R
authors.lastname: Zhao
authors.affiliation: Medical School of Nantong University, Nantong, 226001, Jiangsu, China.
authors.forename: Huiqun
authors.initials: H
authors.lastname: Wu
authors.affiliation: Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, 210000, Jiangsu, China.
authors.forename: Luo
authors.initials: L
authors.lastname: Gu
authors.affiliation: Department of Thoracic Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210000, Jiangsu, China.
authors.forename: Yijiang
authors.initials: Y
authors.lastname: Chen
mesh_terms: D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects / Q000502:physiology; D049109:Cell Proliferation / Q000187:drug effects / Q000502:physiology; D015536:Down-Regulation / Q000187:drug effects; D004938:Esophageal Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism* / Q000494:pharmacology; D006801:Humans; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D034622:RNA Interference; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D016222:Fibroblast Growth Factor 2; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt
keywords: ECA109; FGF2; PI3K/Akt signalling pathway; esophageal cancer; invasion; migration