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. 2017 Sep 28;14(6):6477–6484. doi: 10.3892/ol.2017.7095

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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 3. — HNF-4α promotes VCR-induced apoptosis and Bcl-2 expression in gastric cancer cells. (A) Gastric cancer cells and their variants were treated with VCR and cell apoptosis was evaluated using an Annexin V-fluorescein isothiocyanate assay and flow cytometry. (B) The expression of total and cleaved caspase-3 in VCR-treated gastric cancer cells was evaluated using western blotting. (C) The expression of Bcl-2 and Baxin gastric cancer cell variants was detected by western blotting. (D) The expression of Bcl-XL and Bak in gastric cancer cell variants was determined by western blotting. β-actin served as a loading control. Results are representative of 3 independent experiments. Ctrl, control; HNF4, hepatocyte nuclear factor 4; VCR, vincristine; Bcl-2, B-cell lymphoma 2; Bax, Bcl-associated X protein; Bcl-XL, B-cell lymphoma extra-large.