lncRNA ACTA2-AS1 predicts malignancy and poor prognosis of triple-negative breast cancer and regulates tumor progression via modulating miR-532-5p.

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
Yi Peng, Xiaoxi Huang, Hongmei Wang
{"title":"lncRNA ACTA2-AS1 predicts malignancy and poor prognosis of triple-negative breast cancer and regulates tumor progression via modulating miR-532-5p.","authors":"Yi Peng,&nbsp;Xiaoxi Huang,&nbsp;Hongmei Wang","doi":"10.1186/s12860-022-00432-7","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Dysregulation of ACTA2-AS1 and miR-532-5p and their functions in various cancers have been widely reported. Their potential of serving as biomarkers in triple-negative breast cancer (TNBC) remains unknown. This study aimed to evaluate the function of ACTA2-AS1 and miR-532-5p and their potential of serving as biomarkers in TNBC.</p><p><strong>Results: </strong>The TNBC tissues were collected from 119 patients, where the reduced level of ACTA2-AS1 and increased level of miR-532-5p were observed by PCR and showed a significantly negative correlation (P <  0.001). Both ACTA2-AS1 and miR-532-5p were closely associated with the malignant development and poor prognosis of TNBC patients. Moreover, in TNBC cell, overexpressing ACTA2-AS1 was found to suppress cell proliferation and metastasis, which was reversed by the upregulation of miR-532-5p.</p><p><strong>Conclusions: </strong>ACTA2-AS1 and miR-532-5p could act as biomarkers of TNBC predicting the progression and prognosis of patients. ACTA2-AS1 served as a tumor suppressor of TNBC which was mediated by miR-532-5p.</p>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2022-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9327331/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s12860-022-00432-7","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Dysregulation of ACTA2-AS1 and miR-532-5p and their functions in various cancers have been widely reported. Their potential of serving as biomarkers in triple-negative breast cancer (TNBC) remains unknown. This study aimed to evaluate the function of ACTA2-AS1 and miR-532-5p and their potential of serving as biomarkers in TNBC.

Results: The TNBC tissues were collected from 119 patients, where the reduced level of ACTA2-AS1 and increased level of miR-532-5p were observed by PCR and showed a significantly negative correlation (P <  0.001). Both ACTA2-AS1 and miR-532-5p were closely associated with the malignant development and poor prognosis of TNBC patients. Moreover, in TNBC cell, overexpressing ACTA2-AS1 was found to suppress cell proliferation and metastasis, which was reversed by the upregulation of miR-532-5p.

Conclusions: ACTA2-AS1 and miR-532-5p could act as biomarkers of TNBC predicting the progression and prognosis of patients. ACTA2-AS1 served as a tumor suppressor of TNBC which was mediated by miR-532-5p.

Abstract Image

Abstract Image

Abstract Image

lncRNA ACTA2-AS1可预测三阴性乳腺癌的恶性和不良预后,并通过调节miR-532-5p调控肿瘤进展。
背景:ACTA2-AS1和miR-532-5p的失调及其在各种癌症中的功能已经被广泛报道。它们作为三阴性乳腺癌(TNBC)生物标志物的潜力尚不清楚。本研究旨在评估ACTA2-AS1和miR-532-5p的功能及其作为TNBC生物标志物的潜力。结果:收集119例TNBC患者的TNBC组织,通过PCR观察到ACTA2-AS1水平降低,miR-532-5p水平升高,并呈显著负相关(P)结论:ACTA2-AS1和miR-532-5p可作为TNBC的生物标志物,预测患者的进展和预后。ACTA2-AS1作为TNBC的抑瘤因子,miR-532-5p介导。
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 求助全文
来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
×
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