The mechanisms of tumor necrosis factor α in regulating Krüpple-like factor 4 expression in SK-BR-3 breast cancer cells.

IF 1.4 4区 医学 Q4 ONCOLOGY Asia-Pacific journal of clinical oncology Pub Date : 2024-01-18 DOI:10.1111/ajco.14046
Caiyun Liu, Chengbao Feng, Haifei Li, Erying Zhang, Bo Liu, Ying Wang, Peng Wang
{"title":"The mechanisms of tumor necrosis factor α in regulating Krüpple-like factor 4 expression in SK-BR-3 breast cancer cells.","authors":"Caiyun Liu, Chengbao Feng, Haifei Li, Erying Zhang, Bo Liu, Ying Wang, Peng Wang","doi":"10.1111/ajco.14046","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To explore the expression and functional role of Krüpple-like factor 4 (KLF4) protein stimulated by tumor necrosis factor α (TNF-α) in SK-BR-3 breast cancer cells.</p><p><strong>Methods: </strong>SK-BR-3 cells were stimulated with various concentrations of TNF-α at 0, 1, 5, 10, and 20 ng/mL. Expression levels of KLF4 protein were detected by Western blotting. In the detection of apoptosis, flow cytometry, and DAPI staining were used for detecting the level of apoptosis.</p><p><strong>Results: </strong>KLF4 expression was markedly elevated following stimulation of SK-BR-3 with TNF-α. At the same time, the expression of KLF4 protein increased gradually with the increase of TNF-α stimulation concentration. TNF-α stimulation of SK-BR-3 cells increased apoptosis as measured by apoptosis levels. By overexpressing KLF4 protein in SK-BR-3 cells, it similarly increased apoptosis and promoted cell death of SK-BR-3 cells.</p><p><strong>Conclusion: </strong>TNF-α promotes KLF4 expression, while TNF-α promotes apoptosis in SK-BR-3 cells, a process that may be due to elevated KLF4 protein expression.</p>","PeriodicalId":8633,"journal":{"name":"Asia-Pacific journal of clinical oncology","volume":null,"pages":null},"PeriodicalIF":1.4000,"publicationDate":"2024-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Asia-Pacific journal of clinical oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/ajco.14046","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Objective: To explore the expression and functional role of Krüpple-like factor 4 (KLF4) protein stimulated by tumor necrosis factor α (TNF-α) in SK-BR-3 breast cancer cells.

Methods: SK-BR-3 cells were stimulated with various concentrations of TNF-α at 0, 1, 5, 10, and 20 ng/mL. Expression levels of KLF4 protein were detected by Western blotting. In the detection of apoptosis, flow cytometry, and DAPI staining were used for detecting the level of apoptosis.

Results: KLF4 expression was markedly elevated following stimulation of SK-BR-3 with TNF-α. At the same time, the expression of KLF4 protein increased gradually with the increase of TNF-α stimulation concentration. TNF-α stimulation of SK-BR-3 cells increased apoptosis as measured by apoptosis levels. By overexpressing KLF4 protein in SK-BR-3 cells, it similarly increased apoptosis and promoted cell death of SK-BR-3 cells.

Conclusion: TNF-α promotes KLF4 expression, while TNF-α promotes apoptosis in SK-BR-3 cells, a process that may be due to elevated KLF4 protein expression.

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
肿瘤坏死因子α调节SK-BR-3乳腺癌细胞中Krüpple样因子4表达的机制
目的探讨肿瘤坏死因子α(TNF-α)刺激的Krüpple样因子4(KLF4)蛋白在SK-BR-3乳腺癌细胞中的表达和功能作用:用不同浓度的 TNF-α(0、1、5、10 和 20 ng/mL)刺激 SK-BR-3 细胞。用 Western 印迹法检测 KLF4 蛋白的表达水平。在检测细胞凋亡时,使用流式细胞仪和 DAPI 染色检测细胞凋亡水平:结果:TNF-α刺激SK-BR-3后,KLF4的表达明显升高。同时,随着TNF-α刺激浓度的增加,KLF4蛋白的表达量也逐渐增加。以细胞凋亡水平衡量,TNF-α刺激SK-BR-3细胞会增加细胞凋亡。通过在SK-BR-3细胞中过表达KLF4蛋白,同样增加了细胞凋亡,促进了SK-BR-3细胞的死亡:结论:TNF-α促进KLF4的表达,而TNF-α促进SK-BR-3细胞的凋亡,这一过程可能是由于KLF4蛋白表达的升高。
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
3.40
自引率
0.00%
发文量
175
审稿时长
6-12 weeks
期刊介绍: Asia–Pacific Journal of Clinical Oncology is a multidisciplinary journal of oncology that aims to be a forum for facilitating collaboration and exchanging information on what is happening in different countries of the Asia–Pacific region in relation to cancer treatment and care. The Journal is ideally positioned to receive publications that deal with diversity in cancer behavior, management and outcome related to ethnic, cultural, economic and other differences between populations. In addition to original articles, the Journal publishes reviews, editorials, letters to the Editor and short communications. Case reports are generally not considered for publication, only exceptional papers in which Editors find extraordinary oncological value may be considered for review. The Journal encourages clinical studies, particularly prospectively designed clinical trials.
期刊最新文献
Cancer Clinical Trial Participation Amongst Culturally and Linguistically Diverse Patients in Australia. Issue Information COSA's 51st Annual Scientific Meeting Bridging gaps, building progress, breaking down disparities 13-15 November 2024. COSA's 51st Annual Scientific Meeting Bridging gaps, building progress, breaking down disparities 13-15 November 2024. COSA's 51st Annual Scientific Meeting Bridging gaps, building progress, breaking down disparities 13-15 November 2024.
×
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