Anti-cancer effects of baicalein on cervical carcinoma cells through down-regulation of the ERK/p38/MAPK pathway.

IF 0.8 4区 医学 Q4 ENDOCRINOLOGY & METABOLISM Journal of biological regulators and homeostatic agents Pub Date : 2021-05-01 DOI:10.23812/21-52-A
Y H Luo, L Zhang, M Y Wang, J Fang, J Y Xia, X L Yu
{"title":"Anti-cancer effects of baicalein on cervical carcinoma cells through down-regulation of the ERK/p38/MAPK pathway.","authors":"Y H Luo,&nbsp;L Zhang,&nbsp;M Y Wang,&nbsp;J Fang,&nbsp;J Y Xia,&nbsp;X L Yu","doi":"10.23812/21-52-A","DOIUrl":null,"url":null,"abstract":"<p><p>The objective of this study was to investigate the effects of baicalein on apoptosis of HeLa human cervical cancer (CC) cells and to elucidate the underlying mechanism. HeLa cells were treated with 20, 50, 100, or 200 μmol/L baicalein for 24, 36, and 48 hours, and CCK-8 assays were used to detect cell viability, and flow cytometry was performed to assess apoptosis rate. Reverse-transcription quantitative PCR was used to measure ERK1/2, p38, and JNK mRNA levels in HeLa cells, and western blotting was performed to measure ERK1/2, p38, and JNK protein levels. The CCK-8 assay showed that the OD value of HeLa cells gradually decreased with increasing baicalein concentrations (P < 0.01) and treatment time (P < 0.01). These results indicated a negative time- and dose-dependent effect of baicalein on HeLa cells. Baicalein treatment of HeLa cells significantly increased apoptosis rate (P < 0.01). In HeLa cells treated with 50 or 200 μmol/L baicalein for 24 h, expression levels of ERK1/2 and p38 mRNA were significantly reduced, whereas that of JNK mRNA was increased (P < 0.01). The levels of phosphorylated ERK1/2 and p38 were significantly reduced, and the level of JNK protein was increased (P < 0.01). Taken together, baicalein appeared to exert anti-cancer effects on HeLa cells through induction of apoptosis and regulation of the ERK/p38/mitogen-activated protein kinase pathway.</p>","PeriodicalId":15084,"journal":{"name":"Journal of biological regulators and homeostatic agents","volume":"35 3","pages":"945-952"},"PeriodicalIF":0.8000,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of biological regulators and homeostatic agents","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.23812/21-52-A","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 1

Abstract

The objective of this study was to investigate the effects of baicalein on apoptosis of HeLa human cervical cancer (CC) cells and to elucidate the underlying mechanism. HeLa cells were treated with 20, 50, 100, or 200 μmol/L baicalein for 24, 36, and 48 hours, and CCK-8 assays were used to detect cell viability, and flow cytometry was performed to assess apoptosis rate. Reverse-transcription quantitative PCR was used to measure ERK1/2, p38, and JNK mRNA levels in HeLa cells, and western blotting was performed to measure ERK1/2, p38, and JNK protein levels. The CCK-8 assay showed that the OD value of HeLa cells gradually decreased with increasing baicalein concentrations (P < 0.01) and treatment time (P < 0.01). These results indicated a negative time- and dose-dependent effect of baicalein on HeLa cells. Baicalein treatment of HeLa cells significantly increased apoptosis rate (P < 0.01). In HeLa cells treated with 50 or 200 μmol/L baicalein for 24 h, expression levels of ERK1/2 and p38 mRNA were significantly reduced, whereas that of JNK mRNA was increased (P < 0.01). The levels of phosphorylated ERK1/2 and p38 were significantly reduced, and the level of JNK protein was increased (P < 0.01). Taken together, baicalein appeared to exert anti-cancer effects on HeLa cells through induction of apoptosis and regulation of the ERK/p38/mitogen-activated protein kinase pathway.

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
黄芩素通过下调ERK/p38/MAPK通路对宫颈癌细胞的抗癌作用
本研究旨在探讨黄芩素对HeLa人宫颈癌(CC)细胞凋亡的影响,并探讨其机制。分别用20、50、100、200 μmol/L黄芩素处理HeLa细胞24、36、48 h,采用CCK-8法检测细胞活力,流式细胞术检测细胞凋亡率。采用反转录定量PCR检测HeLa细胞ERK1/2、p38和JNK mRNA水平,western blotting检测ERK1/2、p38和JNK蛋白水平。CCK-8检测显示,随着黄芩素浓度的增加(P < 0.01)和处理时间的延长,HeLa细胞OD值逐渐降低(P < 0.01)。这些结果表明黄芩苷对HeLa细胞具有负的时间和剂量依赖性。黄芩素处理显著提高了HeLa细胞的凋亡率(P < 0.01)。50、200 μmol/L黄芩素处理HeLa细胞24 h后,ERK1/2、p38 mRNA表达量显著降低(P < 0.01), JNK mRNA表达量显著升高(P < 0.01)。磷酸化的ERK1/2和p38蛋白水平显著降低,JNK蛋白水平升高(P < 0.01)。综上所述,黄芩素可能通过诱导HeLa细胞凋亡和调控ERK/p38/丝裂原活化蛋白激酶通路发挥抗癌作用。
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
2.20
自引率
15.60%
发文量
0
审稿时长
6 months
期刊介绍: Journal of Biological Regulators & Homeostatic Agents (IF 1.397) is a peer-reviewed journal published every 2 months. The journal publishes original papers describing research in the fields of experimental and clinical medicine, molecular biology, biochemistry, regulatory molecules, cellular immunology and pharmacology.
期刊最新文献
Targeted regulation of BBOX1-AS1 on miR-361-3p and its effect on the biological function of non-small cell lung cancer cell. Plasma brain natriuretic peptide levels in children with idiopathic epilepsy treated with longterm sodium valproate and oxcarbazepine monotherapy. Silenced fatty acid-binding protein 4 suppresses epithelial-mesenchymal transition of endometriosis via the phosphatidyl inositol 3-kinase/protein kinase B axis. Analysis of long non-coding RNA expression profiles in disuse osteoporosis using microarray and bioinformatics. Identification of miRNAs, mRNAs, lncRNAs, and circRNAs associated with hepatocellular carcinoma recurrence after interferon treatment.
×
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