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Transcriptional changes in lymphoma cells induced by LSD1 depletion

ABSTRACT: Transcriptional changes in lymphoma cells induced by LSD1 depletion

PROVIDER: PRJNA416797 | ENA |

REPOSITORIES: ENA

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Transcriptional changes in lymphoma cells induced by LSD1 depletion

Project description:Using RNA-seq we identified the gene expression changes in lymhpoma cells (OCI-Ly1) expressing LSD1 targeted shRNA and control shRNA

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Transcriptional Changes in Germinal Center (GC) B cells from LSD1 conditional knockout mice

Project description:Using RNA-seq we identified the gene expression changes in GC B cells from LSD1 wild-type or LSD1-deficient mice immunized with T cell dependent antigens (Sheep Red Blood cells)

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Frequent ZNF217 mutations lead to transcriptional deregulation of interferon signal transduction via altered chromatin accessibility in B cell lymphoma (Phospho-Proteome)

Project description:Recent exome-wide studies discovered frequent somatic mutations in the epigenetic modifier ZNF217 in primary mediastinal B cell lymphoma (PMBCL) and related disorders. As functional consequences of ZNF217 alterations remain unknown, we comprehensively evaluated their impact in PMBCL. Targeted sequencing identified genetic lesions affecting ZNF217 in 33% of 157 PMBCL patients. Subsequent gene expression profiling (n=120) revealed changes in cytokine and interferon signal transduction in ZNF217-aberrant PMBCL cases. In vitro, knockout of ZNF217 led to changes in chromatin accessibility interfering with binding motifs for crucial lymphoma-associated transcription factors. This led to disturbed expression of interferon-responsive and inflammation-associated genes, altered cell behavior, and an activated B cell phenotype. Mass spectrometry demonstrates that ZNF217 acts within a histone modifier complex containing LSD1, CoREST and HDAC and interferes with H3K4 methylation and H3K27 acetylation. Concluding, our data suggest non-catalytic activity of ZNF217, which directs histone modifier complex function and controls B cell differentiation-associated patterns of chromatin structure.

2024-01-26 | PXD040928 | Pride

Impact of genetic depletion or pharmacological inhibition of LSD1 on gene expression in ovarian cancer cells [CUT&Tag]

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Impact of genetic depletion or pharmacological inhibition of LSD1 on gene expression in ovarian cancer cells [ATAC-Seq]

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Impact of genetic depletion or pharmacological inhibition of LSD1 on gene expression in ovarian cancer cells [RNA-Seq]

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LSD1/KDM1A Maintains Genome-wide Homeostasis of Transcriptional Enhancers [BrU-Seq]

Project description:We performed BrU-Seq after shRNA mediated depletion of Lsd1 in primary cultures of mouse cortical neurons.

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Frequent ZNF217 mutations lead to transcriptional deregulation of interferon signal transduction via altered chromatin accessibility in B cell lymphoma (Global Proteome and PPI)

2024-01-26 | PXD034337 | Pride

Targeting the scaffolding role of LSD1 (KDM1A) poises acute myeloid leukemia cells for Retinoic Acid induced differentiation

Project description:The histone demethylase LSD1 is deregulated in several tumors, including leukemias, providing the rationale for the clinical use of LSD1 inhibitors. In acute promyelocytic leukemia (APL), pharmacological doses of retinoic acid (RA) induce differentiation of APL cells through degradation of the PML-RAR oncogene. APL cells are resistant to LSD1 inhibition or knock-out, but LSD1 inhibition sensitizes them to physiological doses of RA without altering the stability of PML-RAR, and extends survival of leukemic mice upon RA treatment. Non-enzymatic activities of LSD1 are essential to block differentiation of leukemic cells, while the combination of LSD1 inhibitors (or LSD1 knock-out) with low doses of RA releases a differentiation-associated gene expression program, not strictly dependent on changes in histone H3K4 methylation (known substrate of LSD1). An integrated proteomic/epigenomic/mutational analysis showed that LSD1 inhibitors alter the recruitment of LSD1-containing complexes to chromatin through inhibition of the interaction between LSD1 and GFI1, a relevant transcription factor in hematopoiesis.

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Project description:We screened for the changes in gene expression induced by an LSD1 inhibitor to elucidate the mechanism of its cytotoxic effect on T-cell acute lymphoblastic leukemia (T-ALL).

2017-08-15 | GSE85956 | GEO

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