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. 2017 Aug 10;8(8):e2980. doi: 10.1038/cddis.2017.378

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Copyright © 2017 The Author(s)

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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MUC1 mediates chemoresistance via ABCB1. (a and b) HeLa229/shMUC1-B cells were transiently transfected with ABCB1 plasmids (ABCB1) or vector plasmids (vec), then treated with PTX for 48 h. (a) Western blot was used to identify the expression of ABCB1. (b) CCK8 assay was carried out to test the cell viability of the cells. (c) Western blot was used to identify the expression of ABCB1 in HeLa229/TR/shCTL and HeLa229/TR/shABCB1 cell lines with β-actin as loading control. (d) CCK8 was carried out to identify the cell viability of HeLa229/TR/shABCB1 and its control cell line treated with PTX for 48 h. (e and f) CCK8 assays were applied to analyze the proliferation of HeLa229/TR cells treated with PTX (40 nM) combined with verapamil (25 μg/ml) (e) or zosuquidar (0.2 μM) (f) for indicated days. (g and h) CCK8 assays were applied to analyze the proliferation of NCI-H292/TR cells in the treatment of PTX (20 nM) in combination with verapamil (20 μg/ml) (g) or zosuquidar (2 μM) (h) for indicated days. Data are shown of three independent experiments, mean±S.D. (n=3)