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. 2017 Nov 23;15(2):1621–1629. doi: 10.3892/ol.2017.7476

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Copyright: © Hu 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 6. — Role of the HAX-1-MMP-ROS pathway in DOX-based treatment of MCF-7/R cells. (A) MCF-7/R cells were transfected with RNAs and plasmids for 24 h. Then, the cells were treated with 4 µg/ml DOX for another 48 h in the presence or absence of 5 mM NAC. The mitochondrial membrane potential was analyzed by JC-1 staining. (B) The generation of ROS was measured by DHE staining. (C) The cell viability was determined by MTT assays. *P<0.05 vs. DOX+miR-NC group; ^#P<0.05 vs. DOX+miR-125b group. DOX, doxorubicin; BC, breast cancer; miR, microRNA; MCF-7/R, DOX-resistant MCF-7 cells; NAC, N-acetylcysteine; MMP, mitochondrial membrane potential; ROS, reactive oxygen species; DHE, dihydroethidium.