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Effect of LSD1 Inhibitor ORY-1001 on NCI-H1876 small cell lung cancer cells that are CRISPR-inactivated for ZFP36L1 (sgZFP36L1) or ZFP36L1-WT (sgControl)

ABSTRACT: To investigate the impact of inactivating ZFP36L1 on the transcriptional response to the LSD1 inhibitor ORY-1001 We performed RNA-sequencing on NCI-H1876 sgZFP36L1 or sgControl cells treated with ORY-1001 or DMSO

ORGANISM(S): Homo sapiens

PROVIDER: GSE202112 | GEO | 2022/05/06

REPOSITORIES: GEO

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Effect of LSD1 Inhibitor ORY-1001 on NCI-H1876 small cell lung cancer cells that are CRISPR-inactivated for ZFP36L1 (sgZFP36L1) or ZFP36L1-WT (sgControl)

Project description:Effect of LSD1 Inhibitor ORY-1001 on NCI-H1876 small cell lung cancer cells that are CRISPR-inactivated for ZFP36L1 (sgZFP36L1) or ZFP36L1-WT (sgControl)

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Project description:The lysine-specific demethylase LSD1/KDM1A is a key regulator of stem cell potential in acute myeloid leukemia (AML). Inhibition of its expression or catalytic activity overcomes the differentiation block and reduces colony formation potential. We have developed ORY-1001 as highly potent and selective inhibitor of KDM1A. Treatment of AML cell lines with ORY-1001 induces accumulation of H3K4me2 marks at KDM1A target genes, compromises leukemic stem cell capacity, and provokes blast differentiation. ORY-1001 exhibits potent synergy with standard of care drugs and with inhibitors of other epigenetic targets; reduces tumor growth and extends survival in mouse xenograft models of acute leukemia. To develop tools for use in clinical trials, we selected a panel of surrogate biomarkers for pharmacodynamic analysis based on expression changes in a panel of 24 leukemia cell lines. ORY-1001/RG6016 was the first selective KDM1A inhibitor to enter the clinic and is currently being evaluated in leukemia and solid tumor clinical trials.

2018-08-19 | GSE94567 | GEO

Effects of loss of LSD1 activity on small cell lung cancer cell lines via pharmacological inhibition

Project description:To investigate the effects of loss of LSD1 (KDM1A) on differential gene expression, we treated two cell lines of small cell lung cancer with 1 M LSD1 inhibitor ORY-1001 or vehicle control for 10 days. We then performed gene expression profiling analysis on treated and control cells for each of the two cell lines.

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Silencing of ZFP36L1 using siRNA

Project description:ZFP36L1 is a tandem zinc-finger RNA-binding protein that recognizes conserved Adenylate-Uridylate-rich Elements (AREs) located in 3' untranslated regions (UTRs) to mediate RNA decay. We hypothesized that ZFP36L1 is a negative regulator of a post-transcriptional hub involved in the RNA half-life regulation of cancer-related transcripts. Forced expression of ZFP36L1 in cancer cells markedly reduced cell proliferation in vitro and in vivo; whereas silencing of ZFP36L1 enhanced tumor cell growth. To identify direct downstream targets of ZFP36L1, systematic screening using RNA pull-down of wildtype and mutant ZFP36L1 as well as whole transcriptome sequencing of bladder cancer cells ± tet-on ZFP36L1, was performed. A network of 1,410 genes was identified as potential direct targets of ZFP36L1, including HIF1A, CCND1, and E2F1. ZFP36L1 specifically bound to the 3' UTRs of these targets for RNA degradation, thus suppressing their expression. Collectively, our findings reveal an indispensable role of ZFP36L1 as a post-transcriptional safeguard against aberrant hypoxic signaling and abnormal cell cycle progression.

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Effect of restoring endogenous ZFP36L1 expression in CORL47 SCLC Cells that are CRISPR activated for ZFP36L1 (sgZFP36L1-1 and sgZFP36L1-2) or a non-targeting sgRNA (sgControl)

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Roles of Zfp36l1 and Zfp36l1 in retinal development

Project description:We report our study of the function of two members of the TTP (tristetraprolin) mRNA binding protein family, Zfp36l1 and Zfp36l2, in retinal development. We found that Zfp36l1 and Zfp36l2 were expressed in retinal progenitor cells during development and Müller glial cells and photoreceptors in the mature retina. Our analysis of the mutant retinas showed that, whereas the single knockout retinas appeared largely normal, the double knockout (DKO) retina manifested decreased RPC proliferation and increased differentiation of multiple retinal cell types. RNA-seq analysis not only confirmed the imbalance of proliferation and differentiation in the DKO retina but also revealed Zfp36l1 and Zfp36l2 interact with multiple signaling pathways including the sonic hedgehog pathway and the Notch pathway, to regulate this process.

2021-09-01 | GSE158718 | GEO

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