LncRNA FAM30A Suppresses Proliferation and Metastasis of Colorectal Carcinoma by Blocking the JAK–STAT Signalling

Jin Liu, Shuangyin Han, Yuanbo Cui, Qiuyan Zhao, Yunfei Wang, Tian Li, Xiuling Li
{"title":"LncRNA FAM30A Suppresses Proliferation and Metastasis of Colorectal Carcinoma by Blocking the JAK–STAT Signalling","authors":"Jin Liu,&nbsp;Shuangyin Han,&nbsp;Yuanbo Cui,&nbsp;Qiuyan Zhao,&nbsp;Yunfei Wang,&nbsp;Tian Li,&nbsp;Xiuling Li","doi":"10.1111/jcmm.70421","DOIUrl":null,"url":null,"abstract":"<p>Colorectal carcinoma (CRC) poses a serious risk to global human health. Long non-coding RNAs (LncRNAs) play an important role in the pathogenesis of CRC. There is a scarcity of data about a newly identified lncRNA, FAM30A. Our major objective is to investigate the role of FAM30A in the process of CRC. Gene expression data and correlated clinical information were retrieved and downloaded from public databases to identify differentially expressed genes linked to CRC. The expression of FAM30A was identified in clinical samples and CRC cell lines using via Quantitative Real-time Polymerase Chain Reaction (qPCR) assay also. The survival significance of FAM30A was determined via R package “survival.” Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was performed to identify FAM30A-related signalling pathway. The levels of proteins expression were determined by western blot assay. The effect of FAM30A on CRC cell biological behaviours was evaluated by cell function experiments. FAM30A was identified down-regulated in CRC based on the data from public database. FAM30A had lower expression in CRC clinical samples and cell lines. Low FAM30A expression was positively related to a poor prognosis in CRC patients. After FAM30A was overexpressed, the proliferation, invasion, and migration abilities of CRC cells were decreased, and the rate of CRC cell apoptosis increased. Furthermore, overexpression of FAM30A could block JAK–STAT signalling. FAM30A suppresses proliferative, invasive, and migratory abilities of CRC through blocking JAK–STAT signalling. Thus, it can be a novel biomarker of CRC prognosis.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 4","pages":""},"PeriodicalIF":4.2000,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70421","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/jcmm.70421","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Colorectal carcinoma (CRC) poses a serious risk to global human health. Long non-coding RNAs (LncRNAs) play an important role in the pathogenesis of CRC. There is a scarcity of data about a newly identified lncRNA, FAM30A. Our major objective is to investigate the role of FAM30A in the process of CRC. Gene expression data and correlated clinical information were retrieved and downloaded from public databases to identify differentially expressed genes linked to CRC. The expression of FAM30A was identified in clinical samples and CRC cell lines using via Quantitative Real-time Polymerase Chain Reaction (qPCR) assay also. The survival significance of FAM30A was determined via R package “survival.” Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was performed to identify FAM30A-related signalling pathway. The levels of proteins expression were determined by western blot assay. The effect of FAM30A on CRC cell biological behaviours was evaluated by cell function experiments. FAM30A was identified down-regulated in CRC based on the data from public database. FAM30A had lower expression in CRC clinical samples and cell lines. Low FAM30A expression was positively related to a poor prognosis in CRC patients. After FAM30A was overexpressed, the proliferation, invasion, and migration abilities of CRC cells were decreased, and the rate of CRC cell apoptosis increased. Furthermore, overexpression of FAM30A could block JAK–STAT signalling. FAM30A suppresses proliferative, invasive, and migratory abilities of CRC through blocking JAK–STAT signalling. Thus, it can be a novel biomarker of CRC prognosis.

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
LncRNA FAM30A通过阻断JAK-STAT信号传导抑制结直肠癌的增殖和转移
结直肠癌(CRC)对全球人类健康构成严重威胁。长链非编码rna (LncRNAs)在结直肠癌的发病机制中发挥着重要作用。关于新发现的lncRNA FAM30A的数据缺乏。我们的主要目的是研究FAM30A在结直肠癌过程中的作用。从公共数据库中检索和下载基因表达数据和相关临床信息,以鉴定与结直肠癌相关的差异表达基因。FAM30A在临床样品和结直肠癌细胞系中的表达也通过定量实时聚合酶链反应(qPCR)检测。FAM30A的生存意义通过R包“生存”来确定。京都基因与基因组百科全书(KEGG)富集分析鉴定fam30a相关信号通路。western blot法检测蛋白表达水平。通过细胞功能实验评估FAM30A对结直肠癌细胞生物学行为的影响。基于公共数据库的数据,我们发现FAM30A在CRC中下调。FAM30A在结直肠癌临床样本和细胞系中表达较低。FAM30A低表达与CRC患者预后不良呈正相关。FAM30A过表达后,CRC细胞的增殖、侵袭和迁移能力降低,CRC细胞凋亡率升高。此外,FAM30A过表达可阻断JAK-STAT信号传导。FAM30A通过阻断JAK-STAT信号传导抑制CRC的增殖、侵袭和迁移能力。因此,它可能成为结直肠癌预后的一种新的生物标志物。
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
CiteScore
11.50
自引率
0.00%
发文量
0
期刊介绍: The Journal of Cellular and Molecular Medicine serves as a bridge between physiology and cellular medicine, as well as molecular biology and molecular therapeutics. With a 20-year history, the journal adopts an interdisciplinary approach to showcase innovative discoveries. It publishes research aimed at advancing the collective understanding of the cellular and molecular mechanisms underlying diseases. The journal emphasizes translational studies that translate this knowledge into therapeutic strategies. Being fully open access, the journal is accessible to all readers.
期刊最新文献
Issue Information The SGLT2 Inhibitor Canagliflozin Promotes β-Cell Regeneration and Restores and Stabilises β-Cell Identity in a Polygenic Model of Severe Early-Onset Type 2 Diabetes Correction to “Protectin DX Promotes Epithelial Injury Repair and Inhibits Fibroproliferation Partly via ALX/PI3K Signalling Pathway” Correction to “4-Octyl Itaconate Alleviates Cisplatin-Induced Ferroptosis Possibly via Activating the NRF2/HO-1 Signaling Pathway” A Brain-Targeting Curcumin Analog Inhibits Glioblastoma Progression Through THBS1/TGF-β1/PI3K–AKT Axis Modulation: Evidence From Experimental and Bioinformatic Analyses
×
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:604180095
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