治疗口腔鳞状细胞癌的新靶点:Circ_0046336。

IF 1.8 4区 医学 Q4 ENGINEERING, BIOMEDICAL
Jijun Chen, Liang Wang, Danhua Ma, Hongyan Gao, Yuyuan Shi
{"title":"治疗口腔鳞状细胞癌的新靶点:Circ_0046336。","authors":"Jijun Chen, Liang Wang, Danhua Ma, Hongyan Gao, Yuyuan Shi","doi":"10.1177/09287329251363708","DOIUrl":null,"url":null,"abstract":"<p><p>BackgroundThis study was designed to investigate the mechanism of Circ_0046336 in oral squamous cell carcinoma (OSCC).MethodsThe expression pattern of Circ_0046336 and its distribution in OSCC cell lines (SCC-9 and CAL-27) were identified. Fluorescence <i>in situ</i> hybridization was applied to determine the location of Circ_0046336. Circ_0046336 silencing was detected by methylthiazolyldiphenyl-tetrazolium bromide (MTT), flow cytometry and transwell assays. The binding relation between Circ_0046336 and miR-181d-3p or ADAM12 and miR-181d-3p was investigated using bioinformatics and dual luciferase reporter assay. ADAM12 and miR-181d-3p expressions in OSCC cells with Circ_0046336 knockdown were quantified. Rescue assays were carried out, and the expressions of epithelial-mesenchymal transition (EMT)-related proteins were measured via Western blot.ResultsCirc_0046336 was overexpressed and mainly distributed in the cytoplasm of OSCC cells. Circ_0046336 targeted miR-181d-3p and miR-181d-3p targeted ADAM12 in OSCC cells. Circ_0046336 silencing facilitated apoptosis, and suppressed viability, migration and invasion of OSCC cells, while upregulating miR-181d-3p and downregulating ADAM12. MiR-181d-3p deficiency reversed the regulatory role of Circ_0046336 in biological behaviors of OSCC cells. Circ_0046336 silencing promoted E-cadherin expression and inhibited N-cadherin and Vimentin expressions, but such effects were reversed by miR-181d-3p downregulation.ConclusionCirc_0046336 acts as a ceRNA to regulate apoptosis, migration, invasion and EMT of OSCC cells via miR-181d-3p/ADAM12 axis.</p>","PeriodicalId":48978,"journal":{"name":"Technology and Health Care","volume":" ","pages":"9287329251363708"},"PeriodicalIF":1.8000,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A new target for the treatment of oral squamous cell carcinoma: Circ_0046336.\",\"authors\":\"Jijun Chen, Liang Wang, Danhua Ma, Hongyan Gao, Yuyuan Shi\",\"doi\":\"10.1177/09287329251363708\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>BackgroundThis study was designed to investigate the mechanism of Circ_0046336 in oral squamous cell carcinoma (OSCC).MethodsThe expression pattern of Circ_0046336 and its distribution in OSCC cell lines (SCC-9 and CAL-27) were identified. Fluorescence <i>in situ</i> hybridization was applied to determine the location of Circ_0046336. Circ_0046336 silencing was detected by methylthiazolyldiphenyl-tetrazolium bromide (MTT), flow cytometry and transwell assays. The binding relation between Circ_0046336 and miR-181d-3p or ADAM12 and miR-181d-3p was investigated using bioinformatics and dual luciferase reporter assay. ADAM12 and miR-181d-3p expressions in OSCC cells with Circ_0046336 knockdown were quantified. Rescue assays were carried out, and the expressions of epithelial-mesenchymal transition (EMT)-related proteins were measured via Western blot.ResultsCirc_0046336 was overexpressed and mainly distributed in the cytoplasm of OSCC cells. Circ_0046336 targeted miR-181d-3p and miR-181d-3p targeted ADAM12 in OSCC cells. Circ_0046336 silencing facilitated apoptosis, and suppressed viability, migration and invasion of OSCC cells, while upregulating miR-181d-3p and downregulating ADAM12. MiR-181d-3p deficiency reversed the regulatory role of Circ_0046336 in biological behaviors of OSCC cells. Circ_0046336 silencing promoted E-cadherin expression and inhibited N-cadherin and Vimentin expressions, but such effects were reversed by miR-181d-3p downregulation.ConclusionCirc_0046336 acts as a ceRNA to regulate apoptosis, migration, invasion and EMT of OSCC cells via miR-181d-3p/ADAM12 axis.</p>\",\"PeriodicalId\":48978,\"journal\":{\"name\":\"Technology and Health Care\",\"volume\":\" \",\"pages\":\"9287329251363708\"},\"PeriodicalIF\":1.8000,\"publicationDate\":\"2025-08-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Technology and Health Care\",\"FirstCategoryId\":\"5\",\"ListUrlMain\":\"https://doi.org/10.1177/09287329251363708\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"ENGINEERING, BIOMEDICAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Technology and Health Care","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1177/09287329251363708","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ENGINEERING, BIOMEDICAL","Score":null,"Total":0}
引用次数: 0

摘要

本研究旨在探讨Circ_0046336在口腔鳞状细胞癌(OSCC)中的作用机制。方法鉴定Circ_0046336在OSCC细胞株(SCC-9和CAL-27)中的表达模式及其分布。荧光原位杂交法确定Circ_0046336的位置。采用甲基噻唑基二苯四唑溴化铵(MTT)、流式细胞术和transwell检测Circ_0046336的沉默。利用生物信息学和双荧光素酶报告基因法研究Circ_0046336与miR-181d-3p或ADAM12与miR-181d-3p的结合关系。测定Circ_0046336敲低的OSCC细胞中ADAM12和miR-181d-3p的表达。Western blot检测细胞上皮间质转化(epithelial-mesenchymal transition, EMT)相关蛋白的表达。结果scirc_0046336过表达,主要分布于OSCC细胞的细胞质中。Circ_0046336在OSCC细胞中靶向miR-181d-3p, miR-181d-3p靶向ADAM12。Circ_0046336的沉默促进了细胞凋亡,抑制了OSCC细胞的活力、迁移和侵袭,上调了miR-181d-3p,下调了ADAM12。MiR-181d-3p缺失逆转了Circ_0046336在OSCC细胞生物学行为中的调节作用。Circ_0046336沉默促进E-cadherin表达,抑制N-cadherin和Vimentin表达,但这种作用被miR-181d-3p下调逆转。结论circ_0046336作为ceRNA通过miR-181d-3p/ADAM12轴调控OSCC细胞的凋亡、迁移、侵袭和EMT。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A new target for the treatment of oral squamous cell carcinoma: Circ_0046336.

BackgroundThis study was designed to investigate the mechanism of Circ_0046336 in oral squamous cell carcinoma (OSCC).MethodsThe expression pattern of Circ_0046336 and its distribution in OSCC cell lines (SCC-9 and CAL-27) were identified. Fluorescence in situ hybridization was applied to determine the location of Circ_0046336. Circ_0046336 silencing was detected by methylthiazolyldiphenyl-tetrazolium bromide (MTT), flow cytometry and transwell assays. The binding relation between Circ_0046336 and miR-181d-3p or ADAM12 and miR-181d-3p was investigated using bioinformatics and dual luciferase reporter assay. ADAM12 and miR-181d-3p expressions in OSCC cells with Circ_0046336 knockdown were quantified. Rescue assays were carried out, and the expressions of epithelial-mesenchymal transition (EMT)-related proteins were measured via Western blot.ResultsCirc_0046336 was overexpressed and mainly distributed in the cytoplasm of OSCC cells. Circ_0046336 targeted miR-181d-3p and miR-181d-3p targeted ADAM12 in OSCC cells. Circ_0046336 silencing facilitated apoptosis, and suppressed viability, migration and invasion of OSCC cells, while upregulating miR-181d-3p and downregulating ADAM12. MiR-181d-3p deficiency reversed the regulatory role of Circ_0046336 in biological behaviors of OSCC cells. Circ_0046336 silencing promoted E-cadherin expression and inhibited N-cadherin and Vimentin expressions, but such effects were reversed by miR-181d-3p downregulation.ConclusionCirc_0046336 acts as a ceRNA to regulate apoptosis, migration, invasion and EMT of OSCC cells via miR-181d-3p/ADAM12 axis.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Technology and Health Care
Technology and Health Care HEALTH CARE SCIENCES & SERVICES-ENGINEERING, BIOMEDICAL
CiteScore
2.10
自引率
6.20%
发文量
282
审稿时长
>12 weeks
期刊介绍: Technology and Health Care is intended to serve as a forum for the presentation of original articles and technical notes, observing rigorous scientific standards. Furthermore, upon invitation, reviews, tutorials, discussion papers and minisymposia are featured. The main focus of THC is related to the overlapping areas of engineering and medicine. The following types of contributions are considered: 1.Original articles: New concepts, procedures and devices associated with the use of technology in medical research and clinical practice are presented to a readership with a widespread background in engineering and/or medicine. In particular, the clinical benefit deriving from the application of engineering methods and devices in clinical medicine should be demonstrated. Typically, full length original contributions have a length of 4000 words, thereby taking duly into account figures and tables. 2.Technical Notes and Short Communications: Technical Notes relate to novel technical developments with relevance for clinical medicine. In Short Communications, clinical applications are shortly described. 3.Both Technical Notes and Short Communications typically have a length of 1500 words. Reviews and Tutorials (upon invitation only): Tutorial and educational articles for persons with a primarily medical background on principles of engineering with particular significance for biomedical applications and vice versa are presented. The Editorial Board is responsible for the selection of topics. 4.Minisymposia (upon invitation only): Under the leadership of a Special Editor, controversial or important issues relating to health care are highlighted and discussed by various authors. 5.Letters to the Editors: Discussions or short statements (not indexed).
×
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:604180095
Book学术官方微信