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. 2018 Apr 25;15(6):9757–9765. doi: 10.3892/ol.2018.8572

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Copyright: © Qin 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 4. — Dysfunction of proliferation of G9A-inhibited HCC cells, and arrest of cells in G1 phase. (A and B) G9A was inhibited in HCC cells for 72 h. Cell cycle distribution was analyzed using flow cytometry. Results are the mean ± SD of the percentages of G1, S and G2/M phases. (C) Western blotting of cyclin B1 and p27 in HCC cells treated with its specific inhibitor for the indicated time. β-actin levels are presented as the loading control. Results are the mean ± SD of the relative expression level. 0 h treatment groups compared to the 72 h treatment groups. *P<0.05 and **P<0.01 as indicated. G9A, euchromatic histone-lysine N-methyltransferase; SD, standard deviation; p27, cyclin-dependent kinase inhibitor 1B.