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. 2017 Jul 10;3:17034. doi: 10.1038/cddiscovery.2017.34

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Copyright © 2017 The Author(s)

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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EGCG enhanced ER stress-induced apoptosis by targeting PARP16. Flow cytometry analysis with Annexin V-PI staining was performed to evaluate the percentage of apoptotic cells in EGCG combination with BFA (a) or TUN (b) or BFA/TUN treatment alone induced QGY-7703 WT and PARP16-deficient cells for 24 h. EGCG treatment significantly increased the percentage of apoptotic cells in the QGY-7703 WT cells when compared with that of BFA or TUN treatment alone. While EGCG played little or no role in the percentage of apoptotic cells in the PARP16-deficient cells compared with that of controls. Histograms showing analysis on cell apoptosis results were displayed on the right and data were shown as means±S.D. for the independent experiments. *P<0.05, **P<0.01, ***P<0.001 and NS indicated there was not statistically significant (P>0.05). BFA: 5 μg/ml; TUN: 5 μg/ml; EGCG: 100 μM.