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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: 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)

PROVIDER: PRJNA834740 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19052634_1.fastq.gz	Fastqsanger.gz
	SRR19052634_2.fastq.gz	Fastqsanger.gz
	SRR19052635_1.fastq.gz	Fastqsanger.gz
	SRR19052635_2.fastq.gz	Fastqsanger.gz
	SRR19052636_1.fastq.gz	Fastqsanger.gz

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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: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

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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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ZFP36L1

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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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