Neoplasma Vol.65, No.5, p.701-707, 2018
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Title: Overexpression of EPS8L3 promotes cell proliferation by inhibiting the transactivity of FOXO1 in HCC |
Author: C.X. ZENG, L.Y. TANG, C.Y. XIE, F.X. LI, J.Y. ZHAO, N. JIANG, Z. TONG, S.B. FU, F.J. WEN, W.S. FENG |
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Abstract: The homology of epidermal growth factor receptor pathway substrate 8 (EPS8), EPS8L3, is elevated and significantly enhanced in hepatocellular carcinoma (HCC) tissues and cell lines compared to normal liver tissues and cell lines. MTT and colony formation assays demonstrated that EPS8L3 over-expression induces HCC cell proliferation and silencing reduces it. Further experiments illustrated that over-expressing EPS8L3 promotes p-AKT and Cyclin D1 expression, but inhibits the transcriptional activity of FOXO1. Colony formation assay also demonstrated that AKT inhibitor suppresses the effect of EPS8L3 on proliferation in EPS8L3-over-expressing cells, while AKT restores the proliferation of EPS8L3-silenced cells. This suggests that EPS8L3 promotes proliferation by hyper-activating the AKT signaling pathway and subsequently inhibiting FOXO1 transcriptional activity. Our results provide a new view on EPS8L3 and human HCC progression and therefore EPS8L3 may prove a novel therapeutic target for HCC.
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Keywords: hepatocellular carcinoma, EPS8L3, FOXO1, signaling pathway |
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Published online: 24-Sep-2018
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Year: 2018, Volume: 65, Issue: 5 |
Page From: 701, Page To: 707 |
doi:10.4149/neo_2018_170725N503
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