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The long non-coding NEAT1 is a DNp63 target gene able to modulate epidermal differentiation [microarray]

ABSTRACT: Profile of the genomic binding sites for endogenous NEAT1 in human primary keratinocytes (HEKn) maintanied for six days in high calcium-containing medium. Chromatin was isolated from gluteraldeyde-fixed nuclei of differentiated HEKn and NEAT1-associated D

ORGANISM(S): Homo sapiens

PROVIDER: GSE232654 | GEO | 2023/05/17

REPOSITORIES: GEO

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The long non-coding NEAT1 is a DNp63 target gene able to modulate epidermal differentiation [RNA-seq]

Project description:The transcription factor ΔNp63, a master regulator of epithelial biology, is involved in regulating epithelial stem cell function and maintaining the integrity of stratified epithelial tissues such as the epidermis. To this end, ΔNp63 acts as transcriptional repressor or activator towards a distinct subset of protein-coding genes and microRNAs. However, how and whether ∆Np63 regulates long non-coding RNA (lncRNAs) expression is not known. Here, we identified the lncRNAs NEAT1 and MALAT1 as a bona fide ΔNp63 transcriptional targets. We found that in proliferating human keratinocytes ∆Np63 represses NEAT1 and MALAT1 expression by recruiting the histone deacetylates HDAC1/HDAC2 to the p63 DNA binding site located in the proximal promoter of NEAT1 and MALAT1 genomic loci. Upon induction of differentiation, ∆Np63 down-regulation is associated by a marked increase of NEAT1 RNA levels, resulting in an increased assembly of paraspeckles foci both in vitro and in human skin tissues. RNA-seq analysis associated with global DNA binding profile (ChIRP-seq) revealed that NEAT1 associates with the promoter of key epithelial transcription factors sustaining their expression during epidermal differentiation. These molecular events might explain the inability of NEAT1-depleted keratinocytes to undergo the correct epidermal differentiation program. Remarkably, NEAT1 expression is dysregulated in those skin pathologies characterized by aberrant keratinocytes differentiation such as ichthyosis and psoriasis, suggesting its potential involvement in the pathogenesis of skin disorders.

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The long non-coding NEAT1 is a DNp63 target gene able to modulate epidermal differentiation [ChIRP-seq]

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The long non-coding NEAT1 is a DNp63 target gene able to modulate epidermal differentiation

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2023-05-19 | GSE205961 | GEO

The long non-coding NEAT1 is a DNp63 target gene able to modulate epidermal differentiation

Project description:The long non-coding NEAT1 is a DNp63 target gene able to modulate epidermal differentiation

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The long non-coding NEAT1 is a DNp63 target gene able to modulate epidermal differentiation [microarray]

Project description:The long non-coding NEAT1 is a DNp63 target gene able to modulate epidermal differentiation [microarray]

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The long non-coding NEAT1 is a DNp63 target gene able to modulate epidermal differentiation [ChIRP-seq]

Project description:The long non-coding NEAT1 is a DNp63 target gene able to modulate epidermal differentiation [ChIRP-seq]

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The Long Non-coding RNA NEAT1 is regulated by QKI and forms nuclear paraspeckles in glioma

Project description:The long noncoding RNA (lncRNA) Nuclear Enriched Abundant Transcript 1 (NEAT1) is a lncRNA involved in a variety of human cancers and diseases. The human NEAT1 gene produces two distinct isoforms, NEAT1 Long and NEAT1 Short, through alternative 3’ end formation. NEAT1 Long is an essential factor for nuclear paraspeckle formation, while the role of NEAT1 Short is poorly understood. Previous studies have often failed to distinctly detect the two NEAT1 isoforms and reported controversial NEAT1 dysregulation. Moreover, the molecular mechanisms which underlie the dysregulation of NEAT1 isoforms and their functional importance in tumorigenesis remain poorly characterized. We investigated whether usage of the proximal polyadenylation site (PAS) within the NEAT1 transcript is regulated to govern the biogenesis of NEAT1 isoforms in human glioma cells. We found differential dysregulation of NEAT1 isoforms in patient-derived human glioblastoma multiforme (GBM) stem cells. We further show deletion of the NEAT1 PAS reduced NEAT1 Short and increased NEAT1 Long. We identified the RNA binding protein QKI, a risk factor for glioma, facilitates the utilization of the NEAT1 PAS. We present evidence indicating the imbalance of NEAT1 isoforms correlates with transcriptomic pathway changes. We propose QKI-5 regulates NEAT1 isoform biogenesis through modulating the NEAT1 PAS in human glioma cells.

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The Estrogen receptor alpha regulated NEAT1 long non-coding RNA promotes prostate cancer progression [ChIP-Seq]

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