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. 2018 May 4;8:7050. doi: 10.1038/s41598-018-25340-9

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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2DG + P induces ER stress in PC3 and MDAMB231 cells. PC3 cells and MDAMB231 were left untreated (C) or treated with 2DG (10 mM), propranolol (P) (100 µM) or both together (P+2DG) for the indicated times. (a,b) Electron microscopy comparison of control PC3 vs PC3 treated with 2DG + P (scale bars = 500 nm). The arrows pinpoint the ER structures. In 2DG+P condition ER appears condensed. PC3 (c,d) or MDAMB231 (e,f) cells were investigated for ER stress markers CHOP (c,e) and GRP78 (d,f). Signal quantifications are normalized to Erk1/2 as a control of protein loading. CHOP is drastically increased in cells treated with 2DG+P.