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大黄素通过调节上皮-间质转化抑制干性，从而逆转胰腺癌对吉西他滨的耐药性。

Emodin reverses resistance to gemcitabine in pancreatic cancer by suppressing stemness through regulation of the epithelial‑mesenchymal transition.

作者信息

Wei Weitian, Wang Jiangfeng, Hu Yuqian, Chen Sheng, Liu Jinshi

机构信息

The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Cancer and Basic Medicine, Chinese Academy of Sciences, Hangzhou, Zhejiang 310022, P.R. China.

出版信息

Exp Ther Med. 2022 Nov 16;25(1):7. doi: 10.3892/etm.2022.11706. eCollection 2023 Jan.

DOI:10.3892/etm.2022.11706
PMID:36545274
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9748633/
Abstract

The present study aimed to explore the effects and underlying mechanisms of emodin (Emo) on gemcitabine (GEM)-resistant pancreatic cancer. GEM-resistant SW1990 cells (SW1990/GZ) were established by successively doubling the concentration of GEM. Cell viability was measured using the CCK-8 assay and flow cytometry was used to measure cell apoptosis. Cell migration was assessed using a Transwell assay. Sphere and colony-formation assays were used to evaluate cell self-renewal. The expression levels of epithelial-mesenchymal transition (EMT) and stem cell biomarkers were determined using western blotting. Snail family transcriptional repressor 1 gene (Snail) was overexpressed by transfecting cells with pcDNA3.1-Snail plasmids. A xenograft model was established in nude mice by using SW1990/GZ and Snail-overexpressing SW1990/GZ cells. Proliferation, migration, self-renewal and EMT progression of GEM-treated SW1990/GZ cells were significantly suppressed by Emo treatment, whereas the overexpression of Snail abolished the aforementioned effects. In , the antitumor activity of GEM and the inhibitory effect of GEM against EMT progression and stem-like characteristics were enhanced by treatment with Emo, whilst overexpression of Snail reversed these effects. In conclusion, Emo reversed GEM resistance in pancreatic cancer by suppressing stemness and regulating EMT progression.

摘要

本研究旨在探讨大黄素（Emo）对吉西他滨（GEM）耐药胰腺癌的作用及其潜在机制。通过逐步提高GEM浓度建立GEM耐药的SW1990细胞（SW1990/GZ）。采用CCK-8法检测细胞活力，流式细胞术检测细胞凋亡。采用Transwell法评估细胞迁移。采用球体形成和集落形成试验评估细胞自我更新能力。采用蛋白质免疫印迹法检测上皮-间质转化（EMT）和干细胞生物标志物的表达水平。通过用pcDNA3.1-Snail质粒转染细胞来过表达蜗牛家族转录抑制因子1基因（Snail）。利用SW1990/GZ和过表达Snail的SW1990/GZ细胞在裸鼠中建立异种移植模型。大黄素处理显著抑制了GEM处理的SW1990/GZ细胞的增殖、迁移、自我更新和EMT进程，而Snail的过表达消除了上述作用。在体内，大黄素处理增强了GEM的抗肿瘤活性以及GEM对EMT进程和干细胞样特性的抑制作用，而Snail的过表达则逆转了这些作用。总之，大黄素通过抑制干性和调节EMT进程逆转了胰腺癌对吉西他滨的耐药性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/d63dd5a40e1a/etm-25-01-11706-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/3dc0d6ee317b/etm-25-01-11706-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/64c07b16430d/etm-25-01-11706-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/271eac34d48c/etm-25-01-11706-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/b53a278a3e04/etm-25-01-11706-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/baaefe6982c1/etm-25-01-11706-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/b2e7a13e4b39/etm-25-01-11706-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/abcf62348695/etm-25-01-11706-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/d63dd5a40e1a/etm-25-01-11706-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/3dc0d6ee317b/etm-25-01-11706-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/64c07b16430d/etm-25-01-11706-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/271eac34d48c/etm-25-01-11706-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/b53a278a3e04/etm-25-01-11706-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/baaefe6982c1/etm-25-01-11706-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/b2e7a13e4b39/etm-25-01-11706-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/abcf62348695/etm-25-01-11706-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1d/9748633/d63dd5a40e1a/etm-25-01-11706-g07.jpg

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