E2F4 Promotes Malignant Behaviors of Prostate Cancer Through Activating MUC1 Expression Transcriptionally.

IF 1.4 4区 医学 Q4 ONCOLOGY
Long Cheng, Haichao Yang, Shuoguo Tan, Chongjun Shi, Fanfei Zeng, Weizhong Yang, Weiqin Kong
{"title":"E2F4 Promotes Malignant Behaviors of Prostate Cancer Through Activating MUC1 Expression Transcriptionally.","authors":"Long Cheng, Haichao Yang, Shuoguo Tan, Chongjun Shi, Fanfei Zeng, Weizhong Yang, Weiqin Kong","doi":"10.1111/ajco.14164","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>The malignant features of prostate cancer (PC) threaten the patient's life. MUC1 was observably enhanced in PC. However, the reason for higher MUC1 expression in PC is still unclear and deserves to be further investigated.</p><p><strong>Methods: </strong>The abundance of MUC1 and E2F4 was evaluated using RT-qPCR in PC patients and PC cells. Pearson correlation coefficient analyzed the relationship between E2F4 and MUC1 in tissues from PC patients. Malignant phenotypes were examined using clone formation, scratch tests, transwell, and flow cytometry. The JASPAR website, luciferase activity assay, and ChIP were employed for validating interplays between E2F4 and the MUC1 promoter.</p><p><strong>Results: </strong>MUC1 and E2F4 were abnormally elevated in samples of PC patients and PC cells. MUC1 silencing resulted in suppression of growth and metastasis and promotion of cell apoptosis of PC cells. Additionally, E2F4 could provoke the transcriptional activity of MUC1 to enhance MUC1 expression. Furthermore, E2F4 knockdown inhibited malignant features of PC cells, which was abolished by MUC1 overexpression.</p><p><strong>Conclusion: </strong>Our findings revealed that E2F4 silencing led to the suppression of growth and metastasis and the promotion of cell apoptosis of PC cells through reducing MUC1 expression, which offered targeting molecules for PC treatment.</p>","PeriodicalId":8633,"journal":{"name":"Asia-Pacific journal of clinical oncology","volume":" ","pages":""},"PeriodicalIF":1.4000,"publicationDate":"2025-03-20","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.14164","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

Background: The malignant features of prostate cancer (PC) threaten the patient's life. MUC1 was observably enhanced in PC. However, the reason for higher MUC1 expression in PC is still unclear and deserves to be further investigated.

Methods: The abundance of MUC1 and E2F4 was evaluated using RT-qPCR in PC patients and PC cells. Pearson correlation coefficient analyzed the relationship between E2F4 and MUC1 in tissues from PC patients. Malignant phenotypes were examined using clone formation, scratch tests, transwell, and flow cytometry. The JASPAR website, luciferase activity assay, and ChIP were employed for validating interplays between E2F4 and the MUC1 promoter.

Results: MUC1 and E2F4 were abnormally elevated in samples of PC patients and PC cells. MUC1 silencing resulted in suppression of growth and metastasis and promotion of cell apoptosis of PC cells. Additionally, E2F4 could provoke the transcriptional activity of MUC1 to enhance MUC1 expression. Furthermore, E2F4 knockdown inhibited malignant features of PC cells, which was abolished by MUC1 overexpression.

Conclusion: Our findings revealed that E2F4 silencing led to the suppression of growth and metastasis and the promotion of cell apoptosis of PC cells through reducing MUC1 expression, which offered targeting molecules for PC treatment.

求助全文
约1分钟内获得全文 求助全文
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.
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信