MiRNAs as major players in brain health and disease: current knowledge and future perspectives.

IF 6.1 2区 生物学 Q1 CELL BIOLOGY Cell Death Discovery Pub Date : 2025-01-13 DOI:10.1038/s41420-024-02283-x
Sarika V Kapplingattu, Sujata Bhattacharya, Yogita K Adlakha
{"title":"MiRNAs as major players in brain health and disease: current knowledge and future perspectives.","authors":"Sarika V Kapplingattu, Sujata Bhattacharya, Yogita K Adlakha","doi":"10.1038/s41420-024-02283-x","DOIUrl":null,"url":null,"abstract":"<p><p>MicroRNAs are regulators of gene expression and their dysregulation can lead to various diseases. MicroRNA-135 (MiR-135) exhibits brain-specific expression, and performs various functions such as neuronal morphology, neural induction, and synaptic function in the human brain. Dysfunction of miR-135 has been reported in brain tumors, and neurodegenerative and neurodevelopmental disorders. Several reports show downregulation of miR-135 in glioblastoma, indicating its tumor suppressor role in the pathogenesis of brain tumors. In this review, by performing in silico analysis of molecular targets of miR-135, we reveal the significant pathways and processes modulated by miR-135. We summarize the biological significance, roles, and signaling pathways of miRNAs in general, with a focus on miR-135 in different neurological diseases including brain tumors, and neurodegenerative and neurodevelopmental disorders. We also discuss methods, limitations, and potential of glioblastoma organoids in recapitulating disease initiation and progression. We highlight the promising therapeutic potential of miRNAs as antitumor agents for aggressive human brain tumors including glioblastoma.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"7"},"PeriodicalIF":6.1000,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11729916/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Death Discovery","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41420-024-02283-x","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

MicroRNAs are regulators of gene expression and their dysregulation can lead to various diseases. MicroRNA-135 (MiR-135) exhibits brain-specific expression, and performs various functions such as neuronal morphology, neural induction, and synaptic function in the human brain. Dysfunction of miR-135 has been reported in brain tumors, and neurodegenerative and neurodevelopmental disorders. Several reports show downregulation of miR-135 in glioblastoma, indicating its tumor suppressor role in the pathogenesis of brain tumors. In this review, by performing in silico analysis of molecular targets of miR-135, we reveal the significant pathways and processes modulated by miR-135. We summarize the biological significance, roles, and signaling pathways of miRNAs in general, with a focus on miR-135 in different neurological diseases including brain tumors, and neurodegenerative and neurodevelopmental disorders. We also discuss methods, limitations, and potential of glioblastoma organoids in recapitulating disease initiation and progression. We highlight the promising therapeutic potential of miRNAs as antitumor agents for aggressive human brain tumors including glioblastoma.

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
mirna作为脑健康和疾病的主要参与者:当前的知识和未来的观点。
MicroRNAs是基因表达的调控因子,其失调可导致多种疾病。MicroRNA-135 (MiR-135)具有脑特异性表达,在人脑中具有神经元形态学、神经诱导和突触功能等多种功能。miR-135的功能障碍在脑肿瘤、神经退行性和神经发育障碍中有报道。一些报道显示miR-135在胶质母细胞瘤中下调,表明其在脑肿瘤发病机制中的抑瘤作用。在这篇综述中,通过对miR-135的分子靶点进行硅分析,我们揭示了miR-135调节的重要途径和过程。我们总结了mirna的生物学意义、作用和信号通路,重点关注miR-135在不同神经系统疾病(包括脑肿瘤、神经退行性和神经发育障碍)中的作用。我们还讨论了胶质母细胞瘤类器官在重现疾病发生和进展中的方法、局限性和潜力。我们强调了mirna作为侵袭性人脑肿瘤(包括胶质母细胞瘤)的抗肿瘤药物的治疗潜力。
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
Cell Death Discovery
Cell Death Discovery Biochemistry, Genetics and Molecular Biology-Cell Biology
CiteScore
8.30
自引率
1.40%
发文量
468
审稿时长
9 weeks
期刊介绍: Cell Death Discovery is a multidisciplinary, international, online-only, open access journal, dedicated to publishing research at the intersection of medicine with biochemistry, pharmacology, immunology, cell biology and cell death, provided it is scientifically sound. The unrestricted access to research findings in Cell Death Discovery will foster a dynamic and highly productive dialogue between basic scientists and clinicians, as well as researchers in industry with a focus on cancer, neurobiology and inflammation research. As an official journal of the Cell Death Differentiation Association (ADMC), Cell Death Discovery will build upon the success of Cell Death & Differentiation and Cell Death & Disease in publishing important peer-reviewed original research, timely reviews and editorial commentary. Cell Death Discovery is committed to increasing the reproducibility of research. To this end, in conjunction with its sister journals Cell Death & Differentiation and Cell Death & Disease, Cell Death Discovery provides a unique forum for scientists as well as clinicians and members of the pharmaceutical and biotechnical industry. It is committed to the rapid publication of high quality original papers that relate to these subjects, together with topical, usually solicited, reviews, editorial correspondence and occasional commentaries on controversial and scientifically informative issues.
期刊最新文献
Mechanisms and therapeutic potential of the hedgehog signaling pathway in cancer. Targeting the hERG1/β1 integrin complex in lipid rafts potentiates statins anti-cancer activity in pancreatic cancer. YAP/TAZ-Hippo pathway mediates the tumorigenesis of various cancers through post-translational modification represented by ubiquitination. GTPase GPN3 facilitates cell proliferation and migration in non-small cell lung cancer by impeding clathrin-mediated endocytosis of EGFR. METTL3 regulates autophagy of hypoxia-induced cardiomyocytes by targeting ATG7.
×
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