Luteolin and Quercetin combination therapy: Enhanced inhibition of H157 human lung cancer cells

Yinchuan Wang , Jiacheng Chen , Zhanglong Li , Susu Liu , Yuan Liu , Changyuan Yu , Jiahui Liu , Shihui Wang
{"title":"Luteolin and Quercetin combination therapy: Enhanced inhibition of H157 human lung cancer cells","authors":"Yinchuan Wang ,&nbsp;Jiacheng Chen ,&nbsp;Zhanglong Li ,&nbsp;Susu Liu ,&nbsp;Yuan Liu ,&nbsp;Changyuan Yu ,&nbsp;Jiahui Liu ,&nbsp;Shihui Wang","doi":"10.1016/j.prmcm.2024.100479","DOIUrl":null,"url":null,"abstract":"<div><h3>Introduction</h3><p>Traditional Chinese Medicine (TCM) is renowned for its holistic treatment approach and minimal side effects. Luteolin (LUT) and Quercetin (QUE) each possess notable anticancer properties. This study is the first to elucidate the synergistic anticancer activity of the combination of LUT and QUE (LUT+QUE) against lung cancer.</p></div><div><h3>Methods</h3><p>The synergistic anticancer activity of QUE+LUT was evaluated through the combination index (CI) value by varying the concentrations of QUE and LUT. Network pharmacology analysis was then employed to identify the key targets and crucial signaling pathways for QUE and LUT. Finally, the synergistic anticancer mechanisms of QUE+LUT were elucidated by verifying these core targets and pathways through various experiments, including apoptosis assays, migration assays, ELISA, Western blot and reactive oxygen species (ROS) assays.</p></div><div><h3>Results</h3><p>The key targets identify through network pharmacology analysis include BCL2L1, MMP9, JUN, PTGS2, TP53, AKT1 and CASP3. The crucial pathways are the PI3K-Akt signaling pathway and chemically-induce carcinogenic ROS pathways. Cellular experiments demonstrate that QUE+LUT synergistically induce apoptosis, inhibit cell proliferation, migration and invasion, increase ROS levels and regulate the PI3K-Akt signaling pathway, effectively targeting lung cancer cells.</p></div><div><h3>Discussion</h3><p>The combined therapy of QUE and LUT holds potential as an effective treatment for cancer patients, providing valuable insights for the selection and mechanistic exploration of important anticancer drugs.</p></div>","PeriodicalId":101013,"journal":{"name":"Pharmacological Research - Modern Chinese Medicine","volume":"12 ","pages":"Article 100479"},"PeriodicalIF":0.0000,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667142524001210/pdfft?md5=8267ab890f1ce3457e8d197db7f9a91c&pid=1-s2.0-S2667142524001210-main.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pharmacological Research - Modern Chinese Medicine","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2667142524001210","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Introduction

Traditional Chinese Medicine (TCM) is renowned for its holistic treatment approach and minimal side effects. Luteolin (LUT) and Quercetin (QUE) each possess notable anticancer properties. This study is the first to elucidate the synergistic anticancer activity of the combination of LUT and QUE (LUT+QUE) against lung cancer.

Methods

The synergistic anticancer activity of QUE+LUT was evaluated through the combination index (CI) value by varying the concentrations of QUE and LUT. Network pharmacology analysis was then employed to identify the key targets and crucial signaling pathways for QUE and LUT. Finally, the synergistic anticancer mechanisms of QUE+LUT were elucidated by verifying these core targets and pathways through various experiments, including apoptosis assays, migration assays, ELISA, Western blot and reactive oxygen species (ROS) assays.

Results

The key targets identify through network pharmacology analysis include BCL2L1, MMP9, JUN, PTGS2, TP53, AKT1 and CASP3. The crucial pathways are the PI3K-Akt signaling pathway and chemically-induce carcinogenic ROS pathways. Cellular experiments demonstrate that QUE+LUT synergistically induce apoptosis, inhibit cell proliferation, migration and invasion, increase ROS levels and regulate the PI3K-Akt signaling pathway, effectively targeting lung cancer cells.

Discussion

The combined therapy of QUE and LUT holds potential as an effective treatment for cancer patients, providing valuable insights for the selection and mechanistic exploration of important anticancer drugs.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
木犀草素和槲皮素联合疗法:增强对 H157 人肺癌细胞的抑制作用
导言传统中医(TCM)以其整体治疗方法和最小的副作用而闻名。木犀草素(LUT)和槲皮素(QUE)各自具有显著的抗癌特性。本研究首次阐明了木犀草素和槲皮素复方制剂(LUT+QUE)对肺癌的协同抗癌活性。方法通过改变 QUE 和 LUT 的浓度,用组合指数(CI)值来评估 QUE+LUT 的协同抗癌活性。然后通过网络药理学分析确定QUE和LUT的关键靶点和重要信号通路。结果 通过网络药理学分析确定的关键靶点包括 BCL2L1、MMP9、JUN、PTGS2、TP53、AKT1 和 CASP3。关键通路是 PI3K-Akt 信号通路和化学致癌 ROS 通路。细胞实验证明,QUE+LUT 能协同诱导细胞凋亡,抑制细胞增殖、迁移和侵袭,增加 ROS 水平,调节 PI3K-Akt 信号通路,有效靶向肺癌细胞。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
CiteScore
1.60
自引率
0.00%
发文量
0
期刊最新文献
A mechanistic review on Zanthoxylum species for anti-inflammatory and analgesic potentials Exploring the pharmacological mechanism of Tongluo Qingnao formula in treating acute ischemic stroke: A combined approach of network pharmacology, molecular docking and experimental evidences Effect of Eriobotrya japonica L. (Chinese medicinal plant) on the regulation of lipid metabolism in atherosclerosis-induced mice and in HepG-2 cells Unraveling biomolecules, antidiabetic and antioxidants properties of DelitesTM via pharmacoinformatics and in vitro investigation Acorus gramineus extract decreases cancer stem cell properties and stimulates ROS signaling pathway in HepG2 hepatocellular carcinoma cells
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1