LINC01232 promotes ARNTL2 transcriptional activation and inhibits ferroptosis of CRC cells through p300/H3K27ac.

IF 3 4区医学 Q2 GENETICS & HEREDITY Epigenomics Pub Date : 2024-01-01 Epub Date: 2024-09-13 DOI:10.1080/17501911.2024.2387528

Shengwei Zhuang, Zhekun Huang, Hongkai Fan, Zhirong Wu, Han Liu

{"title":"LINC01232 promotes ARNTL2 transcriptional activation and inhibits ferroptosis of CRC cells through p300/H3K27ac.","authors":"Shengwei Zhuang, Zhekun Huang, Hongkai Fan, Zhirong Wu, Han Liu","doi":"10.1080/17501911.2024.2387528","DOIUrl":null,"url":null,"abstract":"Aim: This study investigated the role of lncRNA LINC01232 in ferroptosis of colorectal cancer (CRC).Materials & methods: Real time quantitative polymerase chain reaction or western blot experiments were performed to examine relevant mRNAs and proteins expression. The kit assays evaluated malondialdehyde, iron, Fe2+ and glutathione levels. ROS levels were verified by flow cytometry. Chromatin immunoprecipitation and RNA immunoprecipitation analysis monitored the correlation among LINC01232, H3K27ac, p300 and ARNTL2.Results: LINC01232 or ARNTL2 knockdown facilitated erastin-induced ferroptosis. The interaction between LINC01232 and p300 resulted in the enhancement of H3K27ac levels at ARNTL2 promoter to promote ARNTL2 transcriptional activity. ARNTL2 overexpression reversed the promoting effect of LINC01232 knockdown on ferroptosis.Conclusion: LINC01232 inhibited the ferroptosis in CRC by epigenetically upregulating the transcriptional activity of ARNTL2.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":"16 15-16","pages":"1097-1115"},"PeriodicalIF":3.0000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11418281/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Epigenomics","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/17501911.2024.2387528","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/9/13 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}

引用次数: 0

Abstract

Aim: This study investigated the role of lncRNA LINC01232 in ferroptosis of colorectal cancer (CRC).Materials & methods: Real time quantitative polymerase chain reaction or western blot experiments were performed to examine relevant mRNAs and proteins expression. The kit assays evaluated malondialdehyde, iron, Fe²⁺ and glutathione levels. ROS levels were verified by flow cytometry. Chromatin immunoprecipitation and RNA immunoprecipitation analysis monitored the correlation among LINC01232, H3K27ac, p300 and ARNTL2.Results: LINC01232 or ARNTL2 knockdown facilitated erastin-induced ferroptosis. The interaction between LINC01232 and p300 resulted in the enhancement of H3K27ac levels at ARNTL2 promoter to promote ARNTL2 transcriptional activity. ARNTL2 overexpression reversed the promoting effect of LINC01232 knockdown on ferroptosis.Conclusion: LINC01232 inhibited the ferroptosis in CRC by epigenetically upregulating the transcriptional activity of ARNTL2.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

LINC01232 通过 p300/H3K27ac 促进 ARNTL2 的转录激活并抑制 CRC 细胞的铁变态反应。

目的：本研究探讨了lncRNA LINC01232在结直肠癌（CRC）铁变态反应中的作用：实时定量聚合酶链反应或 Western 印迹实验检测相关 mRNA 和蛋白质的表达。试剂盒测定评估丙二醛、铁、Fe2+ 和谷胱甘肽水平。流式细胞术验证了 ROS 水平。染色质免疫共沉淀和 RNA 免疫共沉淀分析监测了 LINC01232、H3K27ac、p300 和 ARNTL2 之间的相关性：结果：LINC01232或ARNTL2的敲除促进了麦拉宁诱导的铁蛋白沉积。LINC01232和p300之间的相互作用提高了ARNTL2启动子上的H3K27ac水平，从而促进了ARNTL2的转录活性。ARNTL2的过表达逆转了LINC01232敲除对铁突变的促进作用：结论：LINC01232通过表观遗传学方式上调ARNTL2的转录活性，抑制了CRC的铁变态反应。

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

Epigenomics GENETICS & HEREDITY-

CiteScore

5.80

自引率

2.60%

发文量

审稿时长

>12 weeks

期刊介绍： Epigenomics provides the forum to address the rapidly progressing research developments in this ever-expanding field; to report on the major challenges ahead and critical advances that are propelling the science forward. The journal delivers this information in concise, at-a-glance article formats – invaluable to a time constrained community. Substantial developments in our current knowledge and understanding of genomics and epigenetics are constantly being made, yet this field is still in its infancy. Epigenomics provides a critical overview of the latest and most significant advances as they unfold and explores their potential application in the clinical setting.