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. 2017 Aug 14;7:8091. doi: 10.1038/s41598-017-08547-0

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© The Author(s) 2017

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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Schematic diagram about the anti-NSCLC activity of PT via the stimulation of ERS. Our in vivo and in vitro studies showed that PT treatment could stimulate ERS and upregulate a series of ERS-related molecules (i.e., p-PERK, IRE1, ATF4, CHOP) and promoting the efflux of Ca²⁺ from ER into cytoplasm, thus promoting apoptosis (mechanisms via upregulation of Bax, Caspase 3 and p53 expression, and decrease of Bcl2 level), enhancing ROS generation and MMP depolarization, reducing intracellular GSH levels, and inhibiting the ability of migration and adhesion in NSCLC cells. Moreover, THA treatment can enhance the anticancer activity of PT on NSCLC. PT, pterostilbene; THA, thapsigargin; ERS, endoplasmic reticulum stress; NSCLC, non-small-cell lung cancer; p-PERK, phosphorylated-PKR-like ER kinase; IRE1, inositol-requiring enzyme 1; ATF4, activating transcription factor 4; CHOP, C/EBP-homologous protein; Bcl2, B-cell lymphoma-2; Bax, Bcl2-associated X protein; ROS, reactive oxygen species; GSH, glutathione; MMP, mitochondrial membrane potential.