Emanuele Monteleone, Paola Corrieri, Paolo Provero, Daniele Viavattene, Lorenzo Pulvirenti, Laura Raggi, Elena Carbognin, Marco E Bianchi, Graziano Martello, Salvatore Oliviero, Pier Paolo Pandolfi, Valeria Poli
{"title":"STAT3依赖的长非编码RNA Lncenc1通过稳定KmRNA促进小鼠ES细胞的多能性。","authors":"Emanuele Monteleone, Paola Corrieri, Paolo Provero, Daniele Viavattene, Lorenzo Pulvirenti, Laura Raggi, Elena Carbognin, Marco E Bianchi, Graziano Martello, Salvatore Oliviero, Pier Paolo Pandolfi, Valeria Poli","doi":"10.1093/bfgp/elad045","DOIUrl":null,"url":null,"abstract":"<p><p>Embryonic stem cells (ESCs) preserve the unique ability to differentiate into any somatic cell lineage while maintaining their self-renewal potential, relying on a complex interplay of extracellular signals regulating the expression/activity of pluripotency transcription factors and their targets. Leukemia inhibitory factor (LIF)-activated STAT3 drives ESCs' stemness by a number of mechanisms, including the transcriptional induction of pluripotency factors such as Klf4 and the maintenance of a stem-like epigenetic landscape. However, it is unknown if STAT3 directly controls stem-cell specific non-coding RNAs, crucial to balance pluripotency and differentiation. Applying a bioinformatic pipeline, here we identify Lncenc1 in mouse ESCs as an STAT3-dependent long non-coding RNA that supports pluripotency. Lncenc1 acts in the cytoplasm as a positive feedback regulator of the LIF-STAT3 axis by competing for the binding of microRNA-128 to the 3'UTR of the Klf4 core pluripotency factor mRNA, enhancing its expression. Our results unveil a novel non-coding RNA-based mechanism for LIF-STAT3-mediated pluripotency.</p>","PeriodicalId":55323,"journal":{"name":"Briefings in Functional Genomics","volume":" ","pages":"651-662"},"PeriodicalIF":2.5000,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11428181/pdf/","citationCount":"0","resultStr":"{\"title\":\"STAT3-dependent long non-coding RNA Lncenc1 contributes to mouse ES cells pluripotency via stabilizing Klf4 mRNA.\",\"authors\":\"Emanuele Monteleone, Paola Corrieri, Paolo Provero, Daniele Viavattene, Lorenzo Pulvirenti, Laura Raggi, Elena Carbognin, Marco E Bianchi, Graziano Martello, Salvatore Oliviero, Pier Paolo Pandolfi, Valeria Poli\",\"doi\":\"10.1093/bfgp/elad045\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Embryonic stem cells (ESCs) preserve the unique ability to differentiate into any somatic cell lineage while maintaining their self-renewal potential, relying on a complex interplay of extracellular signals regulating the expression/activity of pluripotency transcription factors and their targets. Leukemia inhibitory factor (LIF)-activated STAT3 drives ESCs' stemness by a number of mechanisms, including the transcriptional induction of pluripotency factors such as Klf4 and the maintenance of a stem-like epigenetic landscape. However, it is unknown if STAT3 directly controls stem-cell specific non-coding RNAs, crucial to balance pluripotency and differentiation. Applying a bioinformatic pipeline, here we identify Lncenc1 in mouse ESCs as an STAT3-dependent long non-coding RNA that supports pluripotency. Lncenc1 acts in the cytoplasm as a positive feedback regulator of the LIF-STAT3 axis by competing for the binding of microRNA-128 to the 3'UTR of the Klf4 core pluripotency factor mRNA, enhancing its expression. Our results unveil a novel non-coding RNA-based mechanism for LIF-STAT3-mediated pluripotency.</p>\",\"PeriodicalId\":55323,\"journal\":{\"name\":\"Briefings in Functional Genomics\",\"volume\":\" \",\"pages\":\"651-662\"},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2024-09-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11428181/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Briefings in Functional Genomics\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1093/bfgp/elad045\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"BIOTECHNOLOGY & APPLIED MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Briefings in Functional Genomics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1093/bfgp/elad045","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
STAT3-dependent long non-coding RNA Lncenc1 contributes to mouse ES cells pluripotency via stabilizing Klf4 mRNA.
Embryonic stem cells (ESCs) preserve the unique ability to differentiate into any somatic cell lineage while maintaining their self-renewal potential, relying on a complex interplay of extracellular signals regulating the expression/activity of pluripotency transcription factors and their targets. Leukemia inhibitory factor (LIF)-activated STAT3 drives ESCs' stemness by a number of mechanisms, including the transcriptional induction of pluripotency factors such as Klf4 and the maintenance of a stem-like epigenetic landscape. However, it is unknown if STAT3 directly controls stem-cell specific non-coding RNAs, crucial to balance pluripotency and differentiation. Applying a bioinformatic pipeline, here we identify Lncenc1 in mouse ESCs as an STAT3-dependent long non-coding RNA that supports pluripotency. Lncenc1 acts in the cytoplasm as a positive feedback regulator of the LIF-STAT3 axis by competing for the binding of microRNA-128 to the 3'UTR of the Klf4 core pluripotency factor mRNA, enhancing its expression. Our results unveil a novel non-coding RNA-based mechanism for LIF-STAT3-mediated pluripotency.
期刊介绍：
Briefings in Functional Genomics publishes high quality peer reviewed articles that focus on the use, development or exploitation of genomic approaches, and their application to all areas of biological research. As well as exploring thematic areas where these techniques and protocols are being used, articles review the impact that these approaches have had, or are likely to have, on their field. Subjects covered by the Journal include but are not restricted to: the identification and functional characterisation of coding and non-coding features in genomes, microarray technologies, gene expression profiling, next generation sequencing, pharmacogenomics, phenomics, SNP technologies, transgenic systems, mutation screens and genotyping. Articles range in scope and depth from the introductory level to specific details of protocols and analyses, encompassing bacterial, fungal, plant, animal and human data.
The editorial board welcome the submission of review articles for publication. Essential criteria for the publication of papers is that they do not contain primary data, and that they are high quality, clearly written review articles which provide a balanced, highly informative and up to date perspective to researchers in the field of functional genomics.
京公网安备 11010802042870号
京ICP备2023020795号-1
分享
求助内容：
应助结果提醒方式：
扫码关注我们
