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SDC1 promotes cisplatin resistance in hepatic carcinoma cells via PI3K-AKT pathway by Liquan Yu; Hong Xu; Song Zhang; Jiangming Chen; Zhongshan Yu is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

What is SDC1 promotes cisplatin resistance in hepatic carcinoma cells via PI3K-AKT pathway about?

This study is to analyze the potential contribution of Syndecan 1 (SDC1) to cisplatin resistance in hepatic carcinoma. Cell proliferation and viability were determined by direct counting and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, respectively. The protein levels of SDC1, p-AKT, AKT and β-actin were quantified by western blotting. The SDC1 transcript abundance was measured by real-time polymerase chain reaction. The relative expression of SDC1 in clinical liver tumor samples was analyzed with immunohistochemistry. SDC1 was up-regulated in cisplatin-resistant HepG2 cells (denoted as HepG2 CR hereafter). SDC1-knockdown re-sensitized HepG2 CR cells to cisplatin treatment. Ectopic over-expression of SDC1 conferred drug resistance to naïve HepG2 cells. PI3K/AKT pathway was over-activated in HepG2 CR cells, and simultaneous administration with PI3K inhibitor greatly surmounted the resistance. We also demonstrated that SDC1 was aberrantly up-regulated in clinical hepatocellular carcinoma samples. Our study highlighted the importance of SDC1-PI3K/AKT signaling in the cisplatin resistance in hepatocellular carcinoma.

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Author

Liquan Yu; Hong Xu; Song Zhang; Jiangming Chen; Zhongshan Yu

Publisher

John Wiley and Sons; Springer-Verlag; Springer Verlag; Springer Science and Business Media LLC; Society for Mining, Metallurgy and Exploration Inc. (ISSN 0914-7470)

Published

2020

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)