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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE205961 | GEO | 2023/05/19

REPOSITORIES: GEO

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Similar Datasets

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

Project description: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

2023-05-17 | GSE232654 | GEO

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.

2023-05-17 | GSE205960 | GEO

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

2023-05-17 | GSE205959 | 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

| PRJNA848649 | ENA

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]

| PRJNA973105 | ENA

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]

| PRJNA848653 | ENA

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

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

| PRJNA848654 | ENA

Inhibition of long non-coding RNA NEAT1 impairs myeloid differentiation in acute promyelocytic leukemia cells.

Project description:BACKGROUND: Acute promyelocytic leukemia (APL) is characterized by the reciprocal translocation t(15;17), which fuses PML with retinoic acid receptor alpha (RAR?). Although PML-RAR? is crucially important for pathogenesis and responsiveness to treatment, the molecular and cellular mechanisms by which PML-RAR? exerts its oncogenic potential have not been fully elucidated. Recent reports have suggested that long non-coding RNAs (lncRNAs) contribute to the precise control of gene expression and are involved in human diseases. Little is known about the role of lncRNA in APL. METHODS: We analyzed NEAT1 expression in APL samples and cell lines by real-time quantitative reverse transcription-PCR (qRT-PCR). The expression of PML-RAR? was measured by Western blot. Cell differentiation was assessed by measuring the surface CD11b antigen expression by flow cytometry analysis. RESULTS: We found that nuclear enriched abundant transcript 1 (NEAT1), a lncRNA essential for the formation of nuclear body paraspeckles, is significantly repressed in de novo APL samples compared with those of healthy donors. We further provide evidence that NEAT1 expression was repressed by PML-RAR?. Furthermore, significant NEAT1 upregulation was observed during all-trans retinoic acid (ATRA)-induced NB4 cell differentiation. Finally, we demonstrate the importance of NEAT1 in myeloid differentiation. We show that reduction of NEAT1 by small interfering RNA (siRNA) blocks ATRA-induced differentiation. CONCLUSIONS: Our results indicate that reduced expression of the nuclear long noncoding RNA NEAT1 may play a role in the myeloid differentiation of APL cells.

| S-EPMC4180842 | biostudies-other

Pan-cancer analysis of long non-coding RNA NEAT1 in various cancers.

Project description:Changes in the abundance and activity of long non-coding RNAs (lncRNAs) have an important impact on the development of cancer. The nuclear paraspeckle assembly transcript 1 (NEAT1) has been reported to be overexpressed in many types of cancer since its discovery. However, inconsistencies exist as NEAT1 can also function as a tumor suppressor in certain types of cancer, such as acute promyelocytic leukemia. Here we systematically describe our current understanding of NEAT1 in tumor initiation and progression. First, we analyzed the expression patterns of NEAT1 in various normal tissues and malignant cancers using data from public data portals, the Genotype-Tissue Expression Project (GTEx) and the Cancer Genome Atlas (TCGA), together with recent progress in the study of NEAT1 in various types of cancer. Second, we discussed the functions and mechanisms of NEAT1 in modulating tumor activity. Then, the upstream transcription factors and downstream microRNA targets of NEAT1 in the transcription cascade of cancers were also summarized. These data highlight the emerging role of NEAT1 in tumorigenesis, and present promising targetable pathways and clinical opportunities for tumor prevention and classifications.

| S-EPMC6146416 | biostudies-literature

The Estrogen receptor alpha regulated NEAT1 long non-coding RNA promotes prostate cancer progression

Project description:This SuperSeries is composed of the SubSeries listed below.

2014-12-01 | GSE43988 | GEO