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. 2014 Nov 26;16:472. doi: 10.1186/s13058-014-0472-0

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© Vaden et al.; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Characterization of C-6-induced endoplasmic reticulum (ER) stress. (A) The anticancer small molecule C-6. (B) A dose-response analysis of C6-treated MCF-7 breast cancer cells and MCF-10A mammary epithelial cells measuring cell viability. Error bars represent the ± standard deviation of three replicates. (C) Analysis of the 20 most differentially expressed (upregulated and downregulated) MCF-7 transcripts following a 3-hour treatment with 30 μM C-6 (in triplicate). Results are plotted as a log₂ ratio of the treated versus control samples. (D) Protein expression analysis of proteins associated with the ER stress response pathway following a time course treatment with 30 μM C-6.