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LSD1 inhibition promotes epithelial differentiation through derepression of fate- determining transcription factors [proliferation vs differentiation]

ABSTRACT: Genome-wide gene expression changes triggered by Ca2+-induced differentiation of epidermal progenitors

ORGANISM(S): Homo sapiens

PROVIDER: GSE133738 | GEO | 2019/08/20

REPOSITORIES: GEO

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LSD1 Inhibition Promotes Epithelial Differentiation through Derepression of Fate-Determining Transcription Factors.

Project description:Self-renewing somatic tissues depend upon the proper balance of chromatin-modifying enzymes to coordinate progenitor cell maintenance and differentiation, disruption of which can promote carcinogenesis. As a result, drugs targeting the epigenome hold significant therapeutic potential. The histone demethylase, LSD1 (KDM1A), is overexpressed in numerous cancers, including epithelial cancers; however, its role in the skin is virtually unknown. Here we show that LSD1 directly represses master epithelial transcription factors that promote differentiation. LSD1 inhibitors block both LSD1 binding to chromatin and its catalytic activity, driving significant increases in H3K4 methylation and gene transcription of these fate-determining transcription factors. This leads to both premature epidermal differentiation and the repression of squamous cell carcinoma. Together these data highlight both LSD1's role in maintaining the epidermal progenitor state and the potential of LSD1 inhibitors for the treatment of keratinocyte cancers, which collectively outnumber all other cancers combined.

| S-EPMC6719800 | biostudies-literature

LSD1 inhibition promotes epithelial differentiation through derepression of fate- determining transcription factors [inhibitors]

Project description:We report the impact of the pharmacological inhibition of the Histone 3 Lysine 4 demethylase (H3K4) LSD1 (KDM1A) enzymatic activity on genome-wide gene expression in normal human epidermal keratinocyte (NHEK)

2019-08-20 | GSE133737 | GEO

LSD1 inhibition promotes epithelial differentiation through derepression of fate- determining transcription factors [ChIP-seq]

Project description:We report the impact of the pharmacological inhibition of the Histone 3 Lysine 4 demethylase (H3K4) LSD1 (KDM1A) enzymatic activity on its binding genome wide and how it impacts genome-wide H3K4me1 and H3K4me2 deposition in Normal Human Epidermal Keratinocytes (NHEK)

2019-08-20 | GSE133560 | GEO

LSD1 inhibition promotes epithelial differentiation through derepression of fate- determining transcription factors

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

2019-08-20 | GSE133766 | GEO

LSD1 inhibition promotes epithelial differentiation through derepression of fate- determining transcription factors [proliferation vs differentiation]

Project description:LSD1 inhibition promotes epithelial differentiation through derepression of fate- determining transcription factors [proliferation vs differentiation]

| PRJNA552360 | ENA

LSD1 inhibition promotes epithelial differentiation through derepression of fate- determining transcription factors

Project description:LSD1 inhibition promotes epithelial differentiation through derepression of fate- determining transcription factors

| PRJNA552480 | ENA

LSD1 inhibition promotes epithelial differentiation through derepression of fate- determining transcription factors [inhibitors]

Project description:LSD1 inhibition promotes epithelial differentiation through derepression of fate- determining transcription factors [inhibitors]

| PRJNA552362 | ENA

LSD1 inhibition promotes epithelial differentiation through derepression of fate- determining transcription factors [ChIP-seq]

Project description:LSD1 inhibition promotes epithelial differentiation through derepression of fate- determining transcription factors [ChIP-seq]

| PRJNA551890 | ENA

The Histone Demethylase LSD1 Regulates B Cell Proliferation and Plasmablast Differentiation.

Project description:B cells undergo epigenetic remodeling as they differentiate into Ab-secreting cells (ASC). LSD1 is a histone demethylase known to decommission active enhancers and cooperate with the ASC master regulatory transcription factor Blimp-1. The contribution of LSD1 to ASC formation is poorly understood. In this study, we show that LSD1 is necessary for proliferation and differentiation of mouse naive B cells (nB) into plasmablasts (PB). Following LPS inoculation, LSD1-deficient hosts exhibited a 2-fold reduction of splenic PB and serum IgM. LSD1-deficient PB exhibited derepression and superinduction of genes involved in immune system processes; a subset of these being direct Blimp-1 target-repressed genes. Cell cycle genes were globally downregulated without LSD1, which corresponded to a decrease in the proliferative capacity of LSD1-deficient activated B cells. PB lacking LSD1 displayed increased histone H3 lysine 4 monomethylation and chromatin accessibility at nB active enhancers and the binding sites of transcription factors Blimp-1, PU.1, and IRF4 that mapped to LSD1-repressed genes. Together, these data show that LSD1 is required for normal in vivo PB formation, distinguish LSD1 as a transcriptional rheostat and epigenetic modifier of B cell differentiation, and identify LSD1 as a factor responsible for decommissioning nB active enhancers.

| S-EPMC6200601 | biostudies-literature

Automated microscope system for determining factors that predict neuronal fate.

Project description:Unraveling cause-and-effect relationships in the nervous system is challenging because some biological processes begin stochastically, take a significant amount of time to unfold, and affect small neuronal subpopulations that can be difficult to isolate and measure. Single-cell approaches are slow, subject to user bias, and sometimes too laborious to achieve sample sizes large enough to detect important effects. Here, we describe an automated imaging and analysis system that enables us to follow the fates of individual cells and intracellular proteins over time. Observations can be quantified in a high-throughput manner with minimal user bias. We have adapted survival analysis methods to determine whether and how factors measured during longitudinal analysis predict a particular biological outcome. The ability to monitor complex processes at single-cell resolution quickly, quantitatively, and over long intervals should have wide applications for biology.

| S-EPMC553329 | biostudies-literature

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