Fatty acid binding protein 4 promotes epithelial-mesenchymal transition in cervical squamous cell carcinoma through AKT/GSK3β/Snail signaling pathway. (5th February 2018)

• Record Type: Journal Article
• Authors: Jin, Jiangbo; Zhang, Ziyu; Zhang, Song; Chen, Xinyu; Chen, Zhen; Hu, Ping; Wang, Jianbin; Xie, Caifeng
• Is Part Of: Molecular and cellular endocrinology. Volume 461(2018)
• Page Start: 155
• Page End: 164
• Publication Date: 2018-02-05
• Subjects: FABP4 -- Cervical cancer -- EMT -- Migration -- AKT/GSK3β/Snail; Endocrinology -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Endocrinology -- Periodicals; Hormones -- Periodicals; Endocrinologie -- Périodiques; Cytology; Endocrinology; Molecular biology; Periodicals; 573.4
• DOI: 10.1016/j.mce.2017.09.005
• Languages: English
• ISSNs: 0303-7207

Abstract

Abstract: Fatty acid binding protein 4 (FABP4) is a member of the fatty acid binding protein family which involved in a variety of biological cellular processes, including tumorigenesis. However, the role of this key adipokine in cervical cancer is still unclear. In this study, we explored the function of FABP4 in cervical cancer and the underlying molecular mechanisms. FABP4 was specifically elevated in tissue samples from patients with cervical squamous cell carcinoma (CSCC) but not with cervical adenocarcinoma, and the level of FABP4 was correlated with E-cadherin and Vimentin expression. In vitro, exogenous FABP4 promoted the migration and invasion of CSCC cells in a dose-dependent manner, and reorganized the actin cytoskeletons in F-Actin staining and TGF-β induced EMT assays. Importantly, the AKT/GSK3β/Snail pathway appears to be involved in FABP4-induced EMT in CSCC cells. In conclusion, our research demonstrated elevated FABP4 promoted EMT via the activation of AKT/GSK3β/Snail pathway in CSCC. Highlights: FABP4 was elevated and correlated with E-cadherin and Vimentin in CSCC tissue. Different subcellular location of FABP4 in CSCC and cervical adenocarcinoma. Exogenous FABP4 specifically promoted the migration and invasion of SiHa cells. Exogenous FABP4 facilitated TGFβ-induced EMT in SiHa cells. Exogenous FABP4 regulated EMT via AKT/GSK3β/Snail signaling pathway.