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

ABSTRACT: LSD1 is frequently overexpressed and correlates with poor prognosis in patients with ovarian cancer. RNA-seq, CUT&Tag-seq and ATAC-seq were performed to determine the impact of genetic depletion or pharmacological inhibition of LSD1 on gene expresion profiles in ovarian cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE218794 | GEO | 2023/10/20

REPOSITORIES: GEO

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

Project description:LSD1 is frequently overexpressed and correlates with poor prognosis in patients with ovarian cancer. RNA-seq, CUT&Tag-seq and ATAC-seq were performed to determine the impact of genetic depletion or pharmacological inhibition of LSD1 on gene expresion profiles in ovarian cancer cells.

2023-10-20 | GSE218795 | GEO

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

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CUT & RUN analysis of H3K4me2 mark upon LSD1 inhibition

Project description:Lysine-specific demethylase 1 (LSD1) is a histone demethylase that promotes stemness and cancer cell survival, including in prostate cancer. LSD1 has been shown to perfrom catalytic independent function sto promote prostate cancer survival. Here, we tested the levels of LSD1's canonical target H3K4me2 upon LSD1 inhibition with SP2509 across the genome using CUT and RUN analysis.

2023-08-30 | GSE235211 | GEO

Transcriptomic maps of pharmacological LSD1 inhibition in MCC [SLAMseq]

Project description:Merkel cell carcinoma (MCC) is a highly aggressive, neuroendocrine skin cancer that lacks actionable mutations, which could be utilized for targeted therapies. Epigenetic regulators governing cell identity may represent unexplored therapeutic entry points. Here, we targeted epigenetic regulators in a pharmacological screen and discovered that the lysine-specific histone demethylase 1A (LSD1/KDM1A) is required for MCC growth in vitro and in vivo. We show that LSD1 inhibition in MCC disrupts the LSD1-CoREST complex leading to displacement and degradation of HMG20B (BRAF35), a poorly characterized complex member that is essential for MCC proliferation. Inhibition of LSD1 causes derepression of transcriptional master regulators of the neuronal lineage, activates a gene expression signature resembling normal Merkel cells, and induces cell cycle arrest and cell death. Our study unveils the importance of LSD1 for proliferation and maintaining cell identity in MCC. There is growing evidence that cancer cells exploit cellular plasticity and dedifferentiation programs to evade destruction by the immune system. The combination of LSD1 inhibitors with checkpoint inhibitors may thus represent a promising treatment strategy for MCC patients.

2020-09-04 | GSE147816 | GEO

Transcriptomic maps of pharmacological LSD1 inhibition in MCC [QUANTseq]

2020-09-04 | GSE147815 | GEO

Chromatin profiling upon pharmacological LSD1 inhibition in MCC [CUT&RUN]

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Genome-wide chromatin accessibility mapping upon pharmacological LSD1 inhibition in MCC [ATACseq]

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LSD1 pharmacological inhibition in SET-2 containing wild type and mutant LSD1 [ChIP-Seq]

Project description:We characterized the changes in histone modifications as well as the localization of LSD1 and GFI1B for both wt SET-2 and drug-resistant SET-2 LSD1 (Leu659_Asn660insArg) treated with GSK-LSD1

2019-01-23 | GSE121424 | GEO

Chromatin profiling upon pharmacological LSD1 inhibition in MCC [CUT&RUN]

Project description:Chromatin profiling upon pharmacological LSD1 inhibition in MCC [CUT&RUN]

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LSD1 pharmacological inhibition in SET-2 containing wild type and mutant LSD1 [RNA-Seq]

Project description:We characterized the effect of GSK-LSD1 treatment on gene expression for both wt SET-2 and drug-resistant SET-2 LSD1 (Leu659_Asn660insArg)

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