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. 2020 Mar 20;56(6):1455–1467. doi: 10.3892/ijo.2020.5023

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Copyright: © Jiao et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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ZEB1-AS1 serves as a competing endogenous RNA and negatively regulates miR-200a expression in IHCC cells. (A) Subcellular localization of ZEB1-AS1 was detected by quantifying nuclear/cytoplasmic RNA fractions. (B) The potential binding site of ZEB1-AS1 and miR-200a predicted by a bioinformatics tool (starBase 2.0). (C) Dual-luciferase reporter assay was performed to detect the binding of miR-200a and ZEB1-AS1. (D) Relative expression levels of miR-200a in HuCCT1 cells with ZEB1-AS1 knockdown, RBE cells with ZEB1-AS1 overexpression and control cells. (E) Spearman's correlation analysis of ZEB1-AS1 and miR-200a in IHCC. (F) Spearman's correlation analysis of miR-200a and E-cadherin in IHCC. ^*P<0.05. ZEB1-AS1, lncRNA ZEB1 antisense 1; IHCC, intrahepatic cholangiocarcinoma.