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. 2017 Sep 25;14(6):6463–6470. doi: 10.3892/ol.2017.7045

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Copyright: © Gan 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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Figure 1. — HMGN5 determines the responses of UBC cell lines to CDDP via the phosphoinositide 3-kinase/Akt signaling pathway. (A) Western blotting of HMGN5 expression in 5637, T24 and UM-UC-3 cell lines. β-actin served as a loading control. (B) Different concentrations of CDDP as indicated were used to treat 5637, T24 and UM-UC-3 cells for dose-dependent cell proliferation MTT assay for 72 h. (C) 5637, T24 and UM-UC-3 cells were infected with lentivirus for HMGN5 depletion or negative control, the expression of HMGN5, Akt and p-Akt was subsequently analyzed by western blotting after 72 h. β-actin served as a loading control. Results are expressed as the mean ± standard deviation (n=3). HMGN5, high mobility group nucleosome-binding domain 5; CDDP, cisplatin; p-, phosphorylated; IC₅₀, Half-maximal inhibitory concentration; sh, short hairpin; Con, control.