Overexpression of E74-Like Factor 5 (ELF5) Inhibits Migration and Invasion of Ovarian Cancer Cells.

Abstract

BackgroundE74-like factor 5 (ELF5) plays a key role in the processes of cell differentiation, apoptosis, and occurrence of tumors. However, the effect of ELF5 on metastasis and invasion in human ovarian cancer remains poorly understood.Material/MethodsQuantitative real-time polymerase chain reaction (qPCR) was performed to measure the expression of ELF5. The viability of cells was detected by cell counting kit (CCK-8). Cell apoptosis was tested by flow cytometry. Matrigel plug angiogenesis assay was employed to determine angiogenesis rate. The protein expression levels of vascular endothelial growth factor (VEGF), cleaved caspase-3, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), E-cadherin, N-cadherin, Snail, phosphoinositide 3 kinase (PI3K), phosphorylated (p)-PI3K, tyrosine kinase B (AKT), and phosphorylated (p)-AKT were determined by Western blot. Wound-healing assay and Transwell were used to determine invasion and migration.ResultsWe found that expression of ELF5 was obviously decreased in ovarian cancer cell lines. The cells viability, invasion and metastasis were inhibited by overexpression ELF5. ELF5 suppressed angiogenesis rate and the expression of VEGF. Changes of the expressions of Bcl-2, cleaved caspase-3 and Bax showed that anti-apoptosis ability was improved by ELF5. ELF5 also repressed N-cadherin and Snail and increased E-cadherin. The expressions of p-PI3K and p-AKT were decreased by ELF5. Further study showed that IGF-I reversed the inhibitory effect of ELF5 on growth and metastasis of SKOV3 cells.ConclusionsOverexpression of ELF5 promoted the apoptosis and reduced the migration and invasion of ovarian cancer cells; therefore, it could provide a new approach to gene treatment of ovarian carcinoma.