DNA methyltransferases‐associated long non‐coding RNA PRKCQ‐AS1 regulate DNA methylation in myelodysplastic syndrome

Author:

Wen Jian1ORCID,Wu Yongbin2,Luo Quanfang1

Affiliation:

1. Department of Hematology Nanxishan Hospital of Guangxi Zhuang Autonomous Region Guilin Guangxi Zhuang Autonomous Region China

2. Department of Laboratory Medicine Nanxishan Hospital of Guangxi Zhuang Autonomous Region Guilin Guangxi Zhuang Autonomous Region China

Abstract

AbstractIntroductionMyelodysplastic syndrome (MDS) is a group of clonal hematopoietic stem cell disorders. DNA hypermethylation is considered to be the key mechanism of pathogenesis for MDS. Studies have demonstrated that DNA methylation can be regulated by the co‐effect between long non‐coding RNAs (lncRNAs) and DNA methyltransferases (DNMTs). The aim of this study was to identify DNMTs‐associated differentially expressed (DE) lncRNAs, which may be a novel diagnostic and therapeutic target for MDS.MethodsTwo gene expression profile datasets (GSE4619 and GSE19429) were downloaded from the Gene Expression Omnibus (GEO) database. Systematic bioinformatics analysis was conducted. Then we verified the expression of PRKCQ‐AS1 in MDS patients and features in SKM‐1 cells.ResultsBioinformatics analysis revealed that the DNMT‐associated DE‐lncRNA PRKCQ‐AS1 was functionally related to DNA methylation. The target genes of PRKCQ‐AS1 associated with DNA methylation are mainly methionine synthetase (MTR) and ten‐eleven‐translocation 1 (TET1). Moreover, the high expression of PRKCQ‐AS1 was verified in real MDS cases. Further cellular analysis in SKM‐1 cells revealed that overexpressed PRKCQ‐AS1 promoted methylation levels of long interspersed nuclear element 1 (LINE‐1) and cell proliferation, and apparently elevated both mRNA and protein levels of MTR and TET1, while knockdown of PRKCQ‐AS1 showed opposite trend in SKM‐1 cells.ConclusionDNMT‐associated DE‐lncRNA PRKCQ‐AS1 may affects DNA methylation levels by regulating MTR and TET1.

Publisher

Wiley

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3