LncRNA ABHD11-AS1 Elevates CALM2 to Promote Metastasis of Thyroid Cancer Through Sponging miR-876-5p.

IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
Juan Lv, Fukun Chen, Ling Lv, Lu Zhang, Huangren Zou, Yanlin Liu, Yuke Bai, Ruotong Fang, Tiantian Qin, Zhiyong Deng
{"title":"LncRNA ABHD11-AS1 Elevates CALM2 to Promote Metastasis of Thyroid Cancer Through Sponging miR-876-5p.","authors":"Juan Lv, Fukun Chen, Ling Lv, Lu Zhang, Huangren Zou, Yanlin Liu, Yuke Bai, Ruotong Fang, Tiantian Qin, Zhiyong Deng","doi":"10.1007/s10528-025-11072-9","DOIUrl":null,"url":null,"abstract":"<p><p>In the past decade, the treatment of thyroid cancer (TC) has been brought to a new era, but tumor metastasis still is an intractable difficulty in clinical. LncRNA ABHD11-AS1 has been confirmed to be involved in TC progression. However, its specific mechanism remains unknown. Tissues from TC patients and TC cells served as mainly experimental subjects in this study. The migration of TC cells was assessed using the scratch assay, and the ability of cell invasion was evaluated by transwell assay. RT-qPCR and western blot were conducted to determine the levels of related genes and proteins. The dual-luciferase reporter assay was used to validate the relationships among ABHD11-AS1, miR-876-5p and CALM2. ABHD11-AS1 and CALM2 are elevated in TC cancer samples and cells, while the expression of miR-876-5p is reduced. Subsequently, the ability of TC cells to migrate, invade and EMT was inhibited by both ABHD11-AS1 knockdown or miR-876-5p overexpression. Moreover, the suppression of malignant characteristics in TC cells resulting from ABHD11-AS knockdown was counteracted by the inhibition of miR-876-5p or the upregulation of CALM2. On the mechanism, ABHD11-AS1 elevated CALM2 and promoted the malignant development of TC cells by acting as a miR-876-5p sponge. ABHD11-AS1 mediated the miR-876-5p/CALM2 axis to drive the metastasis of thyroid cancer.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1000,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochemical Genetics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s10528-025-11072-9","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

In the past decade, the treatment of thyroid cancer (TC) has been brought to a new era, but tumor metastasis still is an intractable difficulty in clinical. LncRNA ABHD11-AS1 has been confirmed to be involved in TC progression. However, its specific mechanism remains unknown. Tissues from TC patients and TC cells served as mainly experimental subjects in this study. The migration of TC cells was assessed using the scratch assay, and the ability of cell invasion was evaluated by transwell assay. RT-qPCR and western blot were conducted to determine the levels of related genes and proteins. The dual-luciferase reporter assay was used to validate the relationships among ABHD11-AS1, miR-876-5p and CALM2. ABHD11-AS1 and CALM2 are elevated in TC cancer samples and cells, while the expression of miR-876-5p is reduced. Subsequently, the ability of TC cells to migrate, invade and EMT was inhibited by both ABHD11-AS1 knockdown or miR-876-5p overexpression. Moreover, the suppression of malignant characteristics in TC cells resulting from ABHD11-AS knockdown was counteracted by the inhibition of miR-876-5p or the upregulation of CALM2. On the mechanism, ABHD11-AS1 elevated CALM2 and promoted the malignant development of TC cells by acting as a miR-876-5p sponge. ABHD11-AS1 mediated the miR-876-5p/CALM2 axis to drive the metastasis of thyroid cancer.

求助全文
约1分钟内获得全文 求助全文
来源期刊
Biochemical Genetics
Biochemical Genetics 生物-生化与分子生物学
CiteScore
3.90
自引率
0.00%
发文量
133
审稿时长
4.8 months
期刊介绍: Biochemical Genetics welcomes original manuscripts that address and test clear scientific hypotheses, are directed to a broad scientific audience, and clearly contribute to the advancement of the field through the use of sound sampling or experimental design, reliable analytical methodologies and robust statistical analyses. Although studies focusing on particular regions and target organisms are welcome, it is not the journal’s goal to publish essentially descriptive studies that provide results with narrow applicability, or are based on very small samples or pseudoreplication. Rather, Biochemical Genetics welcomes review articles that go beyond summarizing previous publications and create added value through the systematic analysis and critique of the current state of knowledge or by conducting meta-analyses. Methodological articles are also within the scope of Biological Genetics, particularly when new laboratory techniques or computational approaches are fully described and thoroughly compared with the existing benchmark methods. Biochemical Genetics welcomes articles on the following topics: Genomics; Proteomics; Population genetics; Phylogenetics; Metagenomics; Microbial genetics; Genetics and evolution of wild and cultivated plants; Animal genetics and evolution; Human genetics and evolution; Genetic disorders; Genetic markers of diseases; Gene technology and therapy; Experimental and analytical methods; Statistical and computational methods.
×
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