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. 2017 Apr 10;6(4):e313. doi: 10.1038/oncsis.2017.13

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Copyright © 2017 The Author(s)

Oncogenesis 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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MnSOD is induced by MCT-1 overexpression, p53 knockdown and EGFR activation. (a) MnSOD expression was examined in MCF-10A cells (control and MCT-1) with (shp53) or without (scramble) p53 depletion. (b) Cellular ROS levels were analyzed in MCF-10A cells with different conditions of p53 and MCT-1 expression upon DMSO or AG1478 treatment. Data represent the mean±s.d. (n=3). **P<0.01; ***P<0.001. (c) MnSOD levels were characterized in the H1299 cells (control and MCT-1) without (pCMV) or with p53 re-expression (pCMV p53). (d) The EGFR phosphorylation and MnSOD levels were assessed when H1299 cells were introducing empty vector, wild-type EGFR and EGFR-activating mutants (L858R and exon19 DEL). (e) MDA-MB231 cells with or without MCT-1 overexpression were assayed. (f) MDA-MB231 cells with or without MCT-1 knockdown were evaluated. The protein amounts were normalized to β-actin or GAPDH, and the phosphorylated EGFR levels were normalized to total EGFR levels before comparison with the comparative controls (lane 1).