Mendelian randomization combined with transcriptomic data reveals LINC00652 as a protective factor against the risk of acute lymphoblastic leukemia.

IF 2.3 4区 医学 Q2 HEMATOLOGY
Haiyan Qi, Jianping Lan, Wensong Wang, Xiaogang Wang
{"title":"Mendelian randomization combined with transcriptomic data reveals LINC00652 as a protective factor against the risk of acute lymphoblastic leukemia.","authors":"Haiyan Qi, Jianping Lan, Wensong Wang, Xiaogang Wang","doi":"10.1080/17474086.2025.2528886","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>LINC00652 plays pivotal roles in acute lymphoblastic leukemia (ALL) a heterogeneous hematological malignancy. Here, we investigated the potential regulatory mechanisms of LINC00652 in ALL.</p><p><strong>Research design and methods: </strong>Genome-wide association study data for LINC00652 were obtained for Mendelian randomization and integrated with RNA sequencing data, Bioinformatics analyses, including weighted gene co-expression network analysis (WGCNA), Spearman or Pearson correlation analysis, function, immune microenvironment, subcellular localization, and competing endogenous RNA (ceRNA) network construction, were employed explore the potential mechanisms of LINC00652 in ALL.</p><p><strong>Results: </strong>LINC00652 exhibited no significant causal relationship with ALL but was identified as a protective factor (<i>p</i> > 0.05). LINC00652 levels were significantly decreased in patients with ALL, while WGCNA demonstrated the significance of black and blue modules for ALL. Seventy-nine messenger RNA (mRNAs) (SYT7) significantly correlated with LINC00652 (<i>p</i> > 0.05) and were enriched in the Janus kinase/signal transducer and activator of transcription (STAT), interleukin 2-STAT5, apoptosis, and adipogenesis pathways. Twenty-eight immune cells infiltrated the ALL, with immature B-cells and gamma delta T-cells significantly associated with LINC00652 expression (<i>p</i> < 0.05). LINC00652 was predominantly cytoplasmic, and a ceRNA network involving LINC00652, 36 microRNAs, and 18 mRNAs were proposed.</p><p><strong>Conclusions: </strong>LINC00652 May protect against ALL and influence its pathogenesis through ceRNA mechanisms.</p>","PeriodicalId":12325,"journal":{"name":"Expert Review of Hematology","volume":" ","pages":"1-14"},"PeriodicalIF":2.3000,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Expert Review of Hematology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/17474086.2025.2528886","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"HEMATOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: LINC00652 plays pivotal roles in acute lymphoblastic leukemia (ALL) a heterogeneous hematological malignancy. Here, we investigated the potential regulatory mechanisms of LINC00652 in ALL.

Research design and methods: Genome-wide association study data for LINC00652 were obtained for Mendelian randomization and integrated with RNA sequencing data, Bioinformatics analyses, including weighted gene co-expression network analysis (WGCNA), Spearman or Pearson correlation analysis, function, immune microenvironment, subcellular localization, and competing endogenous RNA (ceRNA) network construction, were employed explore the potential mechanisms of LINC00652 in ALL.

Results: LINC00652 exhibited no significant causal relationship with ALL but was identified as a protective factor (p > 0.05). LINC00652 levels were significantly decreased in patients with ALL, while WGCNA demonstrated the significance of black and blue modules for ALL. Seventy-nine messenger RNA (mRNAs) (SYT7) significantly correlated with LINC00652 (p > 0.05) and were enriched in the Janus kinase/signal transducer and activator of transcription (STAT), interleukin 2-STAT5, apoptosis, and adipogenesis pathways. Twenty-eight immune cells infiltrated the ALL, with immature B-cells and gamma delta T-cells significantly associated with LINC00652 expression (p < 0.05). LINC00652 was predominantly cytoplasmic, and a ceRNA network involving LINC00652, 36 microRNAs, and 18 mRNAs were proposed.

Conclusions: LINC00652 May protect against ALL and influence its pathogenesis through ceRNA mechanisms.

孟德尔随机化结合转录组学数据显示,LINC00652是对抗急性淋巴细胞白血病风险的保护因子。
背景:LINC00652在急性淋巴细胞白血病(ALL)一种异质性血液系统恶性肿瘤中起关键作用。在这里,我们研究了LINC00652在ALL中的潜在调控机制。研究设计与方法:采用孟德尔随机化方法获取LINC00652的全基因组关联研究数据,结合RNA测序数据,通过加权基因共表达网络分析(WGCNA)、Spearman或Pearson相关分析、功能、免疫微环境、亚细胞定位、竞争内源RNA (ceRNA)网络构建等生物信息学分析,探讨LINC00652在ALL中的潜在机制。结果:LINC00652与ALL无显著的因果关系,但被确定为保护因素(p < 0.05)。LINC00652水平在ALL患者中显著降低,而WGCNA显示出黑色和蓝色模块对ALL的意义。79个信使RNA (SYT7)与LINC00652显著相关(p > 0.05),富集于Janus激酶/信号转导和转录激活因子(STAT)、白细胞介素2-STAT5、细胞凋亡和脂肪生成途径。28个免疫细胞浸润ALL,未成熟b细胞和γ δ t细胞与LINC00652表达显著相关(p结论:LINC00652可能通过ceRNA机制对ALL具有保护作用并影响其发病机制。
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 求助全文
来源期刊
CiteScore
4.70
自引率
3.60%
发文量
98
审稿时长
6-12 weeks
期刊介绍: Advanced molecular research techniques have transformed hematology in recent years. With improved understanding of hematologic diseases, we now have the opportunity to research and evaluate new biological therapies, new drugs and drug combinations, new treatment schedules and novel approaches including stem cell transplantation. We can also expect proteomics, molecular genetics and biomarker research to facilitate new diagnostic approaches and the identification of appropriate therapies. Further advances in our knowledge regarding the formation and function of blood cells and blood-forming tissues should ensue, and it will be a major challenge for hematologists to adopt these new paradigms and develop integrated strategies to define the best possible patient care. Expert Review of Hematology (1747-4086) puts these advances in context and explores how they will translate directly into clinical practice.
×
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:604180095
Book学术官方微信