MicroRNA-498 reduces the proliferation and invasion of colorectal cancer cells via targeting Bcl-2

IF 2.8 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY FEBS Open Bio Pub Date : 2019-11-26 DOI:10.1002/2211-5463.12767
Tongsheng Wang, Ling Ma, Wenxia Li, Lei Ding, Hong Gao
{"title":"MicroRNA-498 reduces the proliferation and invasion of colorectal cancer cells via targeting Bcl-2","authors":"Tongsheng Wang,&nbsp;Ling Ma,&nbsp;Wenxia Li,&nbsp;Lei Ding,&nbsp;Hong Gao","doi":"10.1002/2211-5463.12767","DOIUrl":null,"url":null,"abstract":"<p>Colorectal cancer (CRC) remains a major cause of carcinoma-related deaths worldwide. MicroRNA-498 (miR-498) modulates the development of a variety of biological events, including tumorigenesis. Nevertheless, it is unclear whether miR-498 plays a role in CRC. This study was designed to elucidate the underlying mechanism and role of miR-498 in modulation of the viability and invasiveness of CRC cells. We report that CRC tissues and cells exhibited decreased expression of miR-498, and that overexpression of miR-498 resulted in reduced proliferation of CRC cells, concomitant with increased apoptosis. Furthermore, bioinformatic prediction and dual-luciferase reporter assay revealed that miR-498 targeted the 3′-UTR of Bcl-2 for silencing. However, Bcl-2 overexpression suppressed the proapoptosis of miR-498 on CRC cells. In summary, we describe a possible role of miR-498 in CRC, which may lead to the identification of new targets for treatment of this malignancy.</p>","PeriodicalId":12187,"journal":{"name":"FEBS Open Bio","volume":"10 1","pages":"168-175"},"PeriodicalIF":2.8000,"publicationDate":"2019-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/2211-5463.12767","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"FEBS Open Bio","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/2211-5463.12767","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 9

Abstract

Colorectal cancer (CRC) remains a major cause of carcinoma-related deaths worldwide. MicroRNA-498 (miR-498) modulates the development of a variety of biological events, including tumorigenesis. Nevertheless, it is unclear whether miR-498 plays a role in CRC. This study was designed to elucidate the underlying mechanism and role of miR-498 in modulation of the viability and invasiveness of CRC cells. We report that CRC tissues and cells exhibited decreased expression of miR-498, and that overexpression of miR-498 resulted in reduced proliferation of CRC cells, concomitant with increased apoptosis. Furthermore, bioinformatic prediction and dual-luciferase reporter assay revealed that miR-498 targeted the 3′-UTR of Bcl-2 for silencing. However, Bcl-2 overexpression suppressed the proapoptosis of miR-498 on CRC cells. In summary, we describe a possible role of miR-498 in CRC, which may lead to the identification of new targets for treatment of this malignancy.

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
MicroRNA-498通过靶向Bcl-2减少结直肠癌癌症细胞的增殖和侵袭
癌症(CRC)仍然是全球癌症相关死亡的主要原因。微小RNA‐498(miR‐498)调节包括肿瘤发生在内的各种生物事件的发展。然而,目前尚不清楚miR‐498是否在CRC中发挥作用。本研究旨在阐明miR‐498在调节CRC细胞活力和侵袭性中的潜在机制和作用。我们报道,CRC组织和细胞表现出miR‐498的表达减少,miR‐495的过表达导致CRC细胞增殖减少,同时凋亡增加。此外,生物信息学预测和双荧光素酶报告基因分析显示,miR‐498靶向Bcl‐2的3′-UTR进行沉默。然而,Bcl-2过表达抑制了miR‐498在CRC细胞上的促凋亡作用。总之,我们描述了miR‐498在CRC中的可能作用,这可能导致确定治疗这种恶性肿瘤的新靶点。
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
FEBS Open Bio
FEBS Open Bio BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
5.10
自引率
0.00%
发文量
173
审稿时长
10 weeks
期刊介绍: FEBS Open Bio is an online-only open access journal for the rapid publication of research articles in molecular and cellular life sciences in both health and disease. The journal''s peer review process focuses on the technical soundness of papers, leaving the assessment of their impact and importance to the scientific community. FEBS Open Bio is owned by the Federation of European Biochemical Societies (FEBS), a not-for-profit organization, and is published on behalf of FEBS by FEBS Press and Wiley. Any income from the journal will be used to support scientists through fellowships, courses, travel grants, prizes and other FEBS initiatives.
期刊最新文献
Beyond digital twins: the role of foundation models in enhancing the interpretability of multiomics modalities in precision medicine. Mapping Hsp104 interactions using cross-linking mass spectrometry. Characterisation of the role played by ELMO1, GPR141 and the intergenic polymorphism rs918980 in Fuchs' dystrophy in the Indian population. Piezo1 channels enhance anabolic signaling activation induced by electrical stimulation of cultured myotubes. Identification of inhibitors of the Salmonella FraB deglycase, a drug target.
×
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