Lnc NEAT1通过靶向miR-152-3p/CDK6轴促进黑色素瘤的进展:一项观察性研究

IF 1.3 4区 医学 Q2 MEDICINE, GENERAL & INTERNAL
Ning Ning, Zeyu Tian, Hao Feng, Xing Feng
{"title":"Lnc NEAT1通过靶向miR-152-3p/CDK6轴促进黑色素瘤的进展:一项观察性研究","authors":"Ning Ning, Zeyu Tian, Hao Feng, Xing Feng","doi":"10.1097/MD.0000000000040379","DOIUrl":null,"url":null,"abstract":"<p><p>Long noncoding (Lnc) RNAs are novel regulators in melanoma. Lnc nuclear enriched autosomal transcript 1 (NEAT1) was reportedly upregulated in melanoma; however, the functional roles and mechanisms of Lnc NEAT1 need further investigation. Therefore, we used quantitative real-time PCR to determine the mRNA levels of Lnc NEAT1, miR-152-3p, and cyclin-dependent protein kinase 6 (CDK6). The protein level of CDK6 was determined by Western blot. Cell counting kit 8 and colony formation assays were used to assess cell proliferation. Cell migration was measured by wound healing and Transwell assays. Direct binding of the indicated molecules was verified by an RNA-binding protein immunoprecipitation assay and a dual luciferase reporter assay. The results revealed that Lnc NEAT1 and CDK6 were elevated, while miR-152-3p was downregulated in melanoma. Furthermore, Lnc NEAT1 was positively correlated with CDK6 expression and negatively correlated with miR-152-3p level. Furthermore, Lnc NEAT1 facilitated proliferation, migration, and invasion of melanoma cells. The underlying mechanism is that Lnc NEAT1 serves as a sponge for miR-152-3p to suppress the inhibitory effect of miR-152-3p on CDK6. Furthermore, the miR-152-3p/ CDK6 axis was implicated in the progression of melanoma accelerated by Lnc NEAT1. Taken together, Lnc NEAT1 may promote melanoma development by serving as an endogenous sponge of miR-152-3p, increasing CDK6 expression, and identifying a new target for the treatment of melanoma.</p>","PeriodicalId":18549,"journal":{"name":"Medicine","volume":null,"pages":null},"PeriodicalIF":1.3000,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11537649/pdf/","citationCount":"0","resultStr":"{\"title\":\"Lnc NEAT1 facilitates the progression of melanoma by targeting the miR-152-3p/CDK6 axis: An observational study.\",\"authors\":\"Ning Ning, Zeyu Tian, Hao Feng, Xing Feng\",\"doi\":\"10.1097/MD.0000000000040379\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Long noncoding (Lnc) RNAs are novel regulators in melanoma. Lnc nuclear enriched autosomal transcript 1 (NEAT1) was reportedly upregulated in melanoma; however, the functional roles and mechanisms of Lnc NEAT1 need further investigation. Therefore, we used quantitative real-time PCR to determine the mRNA levels of Lnc NEAT1, miR-152-3p, and cyclin-dependent protein kinase 6 (CDK6). The protein level of CDK6 was determined by Western blot. Cell counting kit 8 and colony formation assays were used to assess cell proliferation. Cell migration was measured by wound healing and Transwell assays. Direct binding of the indicated molecules was verified by an RNA-binding protein immunoprecipitation assay and a dual luciferase reporter assay. The results revealed that Lnc NEAT1 and CDK6 were elevated, while miR-152-3p was downregulated in melanoma. Furthermore, Lnc NEAT1 was positively correlated with CDK6 expression and negatively correlated with miR-152-3p level. Furthermore, Lnc NEAT1 facilitated proliferation, migration, and invasion of melanoma cells. The underlying mechanism is that Lnc NEAT1 serves as a sponge for miR-152-3p to suppress the inhibitory effect of miR-152-3p on CDK6. Furthermore, the miR-152-3p/ CDK6 axis was implicated in the progression of melanoma accelerated by Lnc NEAT1. Taken together, Lnc NEAT1 may promote melanoma development by serving as an endogenous sponge of miR-152-3p, increasing CDK6 expression, and identifying a new target for the treatment of melanoma.</p>\",\"PeriodicalId\":18549,\"journal\":{\"name\":\"Medicine\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.3000,\"publicationDate\":\"2024-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11537649/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1097/MD.0000000000040379\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, GENERAL & INTERNAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/MD.0000000000040379","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0

摘要

长非编码(Lnc)RNA是黑色素瘤的新型调控因子。据报道,Lnc核富集常染色体转录本1(NEAT1)在黑色素瘤中上调;然而,Lnc NEAT1的功能作用和机制还需要进一步研究。因此,我们使用实时定量 PCR 检测了 Lnc NEAT1、miR-152-3p 和细胞周期蛋白依赖性蛋白激酶 6(CDK6)的 mRNA 水平。CDK6 的蛋白水平通过 Western 印迹法测定。细胞计数试剂盒 8 和集落形成试验用于评估细胞增殖。通过伤口愈合和 Transwell 试验测定细胞迁移。通过 RNA 结合蛋白免疫沉淀实验和双荧光素酶报告实验验证了所述分子的直接结合。结果显示,黑色素瘤中的 Lnc NEAT1 和 CDK6 升高,而 miR-152-3p 下调。此外,Lnc NEAT1与CDK6的表达呈正相关,而与miR-152-3p的水平呈负相关。此外,Lnc NEAT1 还能促进黑色素瘤细胞的增殖、迁移和侵袭。其基本机制是 Lnc NEAT1 作为 miR-152-3p 的海绵,抑制了 miR-152-3p 对 CDK6 的抑制作用。此外,miR-152-3p/ CDK6 轴也与 Lnc NEAT1 加速黑色素瘤进展有关。综上所述,Lnc NEAT1可能通过充当miR-152-3p的内源性海绵、增加CDK6的表达来促进黑色素瘤的发展,并为治疗黑色素瘤找到了一个新的靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Lnc NEAT1 facilitates the progression of melanoma by targeting the miR-152-3p/CDK6 axis: An observational study.

Long noncoding (Lnc) RNAs are novel regulators in melanoma. Lnc nuclear enriched autosomal transcript 1 (NEAT1) was reportedly upregulated in melanoma; however, the functional roles and mechanisms of Lnc NEAT1 need further investigation. Therefore, we used quantitative real-time PCR to determine the mRNA levels of Lnc NEAT1, miR-152-3p, and cyclin-dependent protein kinase 6 (CDK6). The protein level of CDK6 was determined by Western blot. Cell counting kit 8 and colony formation assays were used to assess cell proliferation. Cell migration was measured by wound healing and Transwell assays. Direct binding of the indicated molecules was verified by an RNA-binding protein immunoprecipitation assay and a dual luciferase reporter assay. The results revealed that Lnc NEAT1 and CDK6 were elevated, while miR-152-3p was downregulated in melanoma. Furthermore, Lnc NEAT1 was positively correlated with CDK6 expression and negatively correlated with miR-152-3p level. Furthermore, Lnc NEAT1 facilitated proliferation, migration, and invasion of melanoma cells. The underlying mechanism is that Lnc NEAT1 serves as a sponge for miR-152-3p to suppress the inhibitory effect of miR-152-3p on CDK6. Furthermore, the miR-152-3p/ CDK6 axis was implicated in the progression of melanoma accelerated by Lnc NEAT1. Taken together, Lnc NEAT1 may promote melanoma development by serving as an endogenous sponge of miR-152-3p, increasing CDK6 expression, and identifying a new target for the treatment of melanoma.

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
Medicine
Medicine 医学-医学:内科
CiteScore
2.80
自引率
0.00%
发文量
4342
审稿时长
>12 weeks
期刊介绍: Medicine is now a fully open access journal, providing authors with a distinctive new service offering continuous publication of original research across a broad spectrum of medical scientific disciplines and sub-specialties. As an open access title, Medicine will continue to provide authors with an established, trusted platform for the publication of their work. To ensure the ongoing quality of Medicine’s content, the peer-review process will only accept content that is scientifically, technically and ethically sound, and in compliance with standard reporting guidelines.
×
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