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. 2017 Jan 23;13(3):1681–1687. doi: 10.3892/ol.2017.5630

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Copyright: © Ma 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 2. — Targeting CD146 substantially enhanced vorinostat-induced killing in ovarian cancer cells. (A) Ovarian cancer A2780 cells were cultured with control mAb mIgG or AA98, which has been confirmed to significantly knockdown the expression of CD146 by western blot analysis. (B) A2780/SKOV3/Caov3 ovarian cancer cells were exposed to 2.5 µmol/l vorinostat for 72 h and subjected to apoptosis assay for the determination of their drug sensitivity, where each data point represents the mean ± standard error of the mean of 3 replicates. (C) A2780 or (D) SKOV3 cells were treated with 10 µg/ml mAb AA98 or 2.5 µmol/l vorinostat + isotype-matched mIgG, or vorinostat + mAb AA98 for 24 h and then subjected to the soft agar colony-forming assay (*P<0.05). Results are expressed as a percentage of colonies in the DMSO-treated group. Each data point represents the mean ± standard deviation of 3 replicates. CD146, cluster of differentiation 146; mAb, monoclonal antibody; mIgG, monoclonal immunoglobulin G; DMSO, dimethyl sulfoxide; SAHA, suberoylanilide hydroxamic acid.