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Transcriptomic response of LSD1-UTX inhibitor on human breast cancer MCF7 cells

ABSTRACT: Transcriptomic response of LSD1-UTX inhibitor on human breast cancer MCF7 cells

PROVIDER: PRJNA533785 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8931640_1.fastq.gz	Fastqsanger.gz
	SRR8931640_2.fastq.gz	Fastqsanger.gz
	SRR8931641_1.fastq.gz	Fastqsanger.gz
	SRR8931641_2.fastq.gz	Fastqsanger.gz
	SRR8931638_1.fastq.gz	Fastqsanger.gz

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Transcriptomic response of LSD1-UTX inhibitor on human breast cancer MCF7 cells

Project description:In many human cancers, including breast and prostate cancers, LSD1 and other lysine demethylases (KDMs), such as UTX, are co-expressed and co-localize with androgen receptors (AR) and estrogen receptors (ER), suggesting the potential use of hybrid molecules to target histone methylation and therefore to regulate/redirect hormone receptor signaling. Here, we report on the action of a pan-KDM inhibitor (3324), obtained by coupling the chemical properties of tranylcypromine, a known LSD1 inhibitor, with the 2OG competitive moiety developed for JmjC inhibition. The 3324 hybrid molecule displays unique features not exhibited by moieties and well-characterized single inhibitors. The compound efficiently inhibits LSD1 as well as UTX enzymes, inducing significant growth arrest and apoptosis in hormone-responsive cells accompanied by a robust increase in H3K4me2 and H3K27me3. Treatment with 3324 reduces the level of ERα in breast and AR in prostate cancer cells at both transcriptional and non-transcriptional levels, acting as a selective endocrine receptor disruptor (SERD). Treatment with 3324 alters the methylation status of ER-regulated promoter regions, thereby affecting the transcription of genes involved in cell surveillance, death, and immune response. 3324 reduces cell proliferation in ex vivo breast cancers by interfering with hormone receptor signaling and/or receptor stability, as well as in cell models with acquired resistance to endocrine therapies (BT474, C4-2 and C4-2b). Similarly, 3324 displays tumor-selective potential in vivo, in both xenograft and chicken embryo models, with no toxicity and good oral efficacy. This multi-target approach may overcome potential mechanism(s) of resistance caused in part by redundancy and robustness of biological pathways, and find potential application in the treatment of resistant-to-therapy cancers such as those with acquired tamoxifen/enzalutamide resistance.

2020-10-15 | GSE130067 | GEO

Analysis of miRNAs in MCF7 cells regulated by LSD1

Project description:Lysine specific demethylase 1 (LSD1) is an important histone demethylase that mediates metastasis in luminal breast cancer. Thus, the characterization of miRNAs in MCF7 cells regulated by LSD1 is imperative in clarifying intercellular signaling.

2024-03-04 | GSE218200 | GEO

Analysis of exosomal miRNAs in MCF7 cells regulated by LSD1

Project description:Lysine specific demethylase 1 (LSD1) is an important histone demethylase that mediates metastasis in luminal breast cancer. Exosomes play a major role in cell-to-cell communication. Thus, the characterization of miRNAs of exosome in MCF7 cells regulated by LSD1 is imperative in clarifying intercellular signaling.

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LSD1 inhibits the invasion and migration of breast cancer through exosomes

Project description:Metastasis accounts for almost 90% of breast cancer-related fatalities, making it frequent malignancy and the main reason of tumor mortality globally among women. A key player in breast cancer is the histone demethylase lysine-specific demethylase 1 (LSD1). We used LSD1 knockdown MCF7 and T47D cell exosomes to treat breast cancer cells for greatly increasing the invasion and migration of breast cancer cells for evaluating the impact of LSD1 on breast cancer invasion and migration. miR-1290 expression was downregulated in LSD1 knockdown MCF7 exosomes. Furthermore, miR-1290 could control NAT1 expression by looking through the database of miR-1290 target genes. These data provide fresh insights into the biology of breast cancer therapy by demonstrating how the epigenetic factor LSD1 stimulates the breast cancer cells’ invasion and migration via controlling exosomal miRNA.

2024-07-31 | GSE266982 | GEO

RNA-seq of small intestinal organoids treated with an inhibitor for the epigenetic modifier LSD1

Project description:To assess the role of LSD1 in mice small intestinal epithelium, small intestinal organoids were treated with an inhibitor for LSD1 (GSK-LSD1) and compared to untreated organoids. Similar to intestinal epithelium from mice with an intestinal epithelium specific LSD1-KO, paneth cells dissappear upon GSK-LSD1 treatment. We used these sequencing data to show that these small intestinal organoids have a similar phenotype as mice epithelium without LSD1.

2020-11-16 | E-MTAB-9077 | biostudies-arrayexpress

Analysis of miRNAs in MCF7 cells regulated by LSD1

Project description:Analysis of miRNAs in MCF7 cells regulated by LSD1

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Trophoblast stem cells (TSC) global transcriptome in stemness conditions after treatment with Lsd1 inhibitor or induction of Lsd1 depletion [RNA-seq]

Project description:RNA-Seq for Lsd1-deficient TSCs or treated with Lsd1 inhibitor for 24hrs

2017-06-12 | GSE78781 | GEO

Utx interactome in mouse myeloid progenitor cells

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Project description:Lysine-specific demethylase 1 (LSD1) is an epigenetic enzyme that oxidatively cleaves methyl groups from monomethyl and dimethyl Lys4 of histone H3 (H3K4Me1, H3K4Me2) and can contribute to gene silencing. This study describes the design and synthesis of analogs of a monoamine oxidase antidepressant, phenelzine, and their LSD1 inhibitory properties. A novel phenelzine analog (bizine) containing a phenyl-butyrylamide appendage was shown to be a potent LSD1 inhibitor in vitro and was selective versus monoamine oxidases A/B and the LSD1 homolog, LSD2. LSD1 inhibitor bizine was found to be effective at modulating bulk histone methylation in cancer cells, and ChIP-seq experiments revealed a statistically significant overlap in the H3K4 methylation pattern of genes affected by bizine and those altered in LSD1-/- cells. Treatment of two cancer cell lines, LNCaP and H460 with bizine conferred a reduction in proliferation rate, and bizine showed additive to synergistic effects on cell growth when used in combination with two out of five HDAC inhibitors tested. Moreover, neurons exposed to oxidative stress were protected by the presence of bizine, suggesting potential applications in neurodegenerative disease.

2014-11-07 | GSE55089 | GEO

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