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紫檀芪通过激活内质网应激发挥对非小细胞肺癌的抗癌活性。

Pterostilbene exerts anticancer activity on non-small-cell lung cancer via activating endoplasmic reticulum stress.

机构信息

Department of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, 1 Xinsi Road, Xi'an, 710038, China.

Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, 710061, China.

出版信息

Sci Rep. 2017 Aug 14;7(1):8091. doi: 10.1038/s41598-017-08547-0.

DOI:10.1038/s41598-017-08547-0
PMID:28808300
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5556085/
Abstract

Pterostilbene (PT), the natural dimethylated analog of resveratrol (RSV), is a potent anticarcinogen for non-small-cell lung cancer (NSCLC), but its anti-NSCLC mechanisms remain unclear. In this study, we show that PT treatment time- and dose-dependently enhanced the endoplasmic reticulum stress (ERS) signaling (i.e., p-PERK, IRE1, ATF4, CHOP), thus decreasing the cell viability and inducing apoptosis in human PC9 and A549 NSCLC cell lines. Moreover, the decreased migratory and adhesive abilities, downregulation of intracellular glutathione (GSH) level, enhanced reactive oxygen species (ROS) generation, Caspase 3 activity and mitochondrial membrane depolarization were observed in NSCLC cells treated with PT. These effects were reversed by CHOP siRNA which inhibited the ERS signaling pathway, but were promoted by thapsigargin (a classical ERS inducer) in vitro. Besides, in vivo studies also verify that PT exerted anticancer activity by mobilizing ERS signaling and apoptosis-related proteins, and these effects were enhanced by thapsigargin. Therefore, ERS activation may represent a new mechanism of anti-NSCLC action by PT, and a novel therapeutic intervention for lung cancer.

摘要

紫檀芪（PT）是白藜芦醇（RSV）的天然二甲化类似物，是一种有效的非小细胞肺癌（NSCLC）抗癌剂，但它的抗 NSCLC 机制仍不清楚。在这项研究中，我们表明 PT 处理时间和剂量依赖性地增强了内质网应激（ERS）信号（即 p-PERK、IRE1、ATF4、CHOP），从而降低了人 PC9 和 A549 NSCLC 细胞系的细胞活力并诱导细胞凋亡。此外，在 NSCLC 细胞中观察到迁移和黏附能力降低，细胞内谷胱甘肽（GSH）水平下调，活性氧（ROS）生成增加，Caspase 3 活性和线粒体膜去极化，这些作用被抑制 ERS 信号通路的 CHOP siRNA 逆转，但在体外被他普西醇（一种经典的 ERS 诱导剂）促进。此外，体内研究也证实，PT 通过动员 ERS 信号和凋亡相关蛋白发挥抗癌活性，这些作用被他普西醇增强。因此，ERS 激活可能代表了 PT 抗 NSCLC 作用的新机制，为肺癌提供了一种新的治疗干预手段。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/ad711b8391a8/41598_2017_8547_Fig9_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/bbf278d9e857/41598_2017_8547_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/de2cf31b23de/41598_2017_8547_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/2880e4cfc50f/41598_2017_8547_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/ad711b8391a8/41598_2017_8547_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/0fc41d228de1/41598_2017_8547_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/d005d229a461/41598_2017_8547_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/7f57d4c4d71b/41598_2017_8547_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/56fe6fe7c955/41598_2017_8547_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/33b0fe965e20/41598_2017_8547_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/bbf278d9e857/41598_2017_8547_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/de2cf31b23de/41598_2017_8547_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/2880e4cfc50f/41598_2017_8547_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ad/5556085/ad711b8391a8/41598_2017_8547_Fig9_HTML.jpg

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