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Single cell RNA-seq analysis of lung cancer cell lines treated with JTE-607

ABSTRACT: single cell RNA-seq analysis of lung cancer cell lines treated with JTE-607

PROVIDER: PRJNA1209070 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31958401_1.fastq.gz	Fastqsanger.gz
	SRR31958401_2.fastq.gz	Fastqsanger.gz
	SRR31958402_1.fastq.gz	Fastqsanger.gz
	SRR31958402_2.fastq.gz	Fastqsanger.gz
	SRR31958403_1.fastq.gz	Fastqsanger.gz

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single cell RNA-seq analysis of lung cancer cell lines treated with JTE-607

Project description:To assess the impact of CPA inhibition by JTE-607 on intra-cell-line transcriptomic heterogeneity, we profiled two lung cancer cell lines treated with DMSO or JTE-607 by 3' tag-based single-cell RNA-seq with 10x Chromium. For data analysis, we performed transcriptome quantification at the PAS-based transcript level to generate a PAS-by-cell count matrix, and then investigate the effect of JTE-607 treatment on PAS usage pattern and cellular states.

2025-01-14 | GSE286399 | GEO

RNA-seq of dTAG-NUDT21 HCT116 cells treated with DMSO+JTE-607 or dTAGV1+JTE-607.

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scRNA-seq analysis of patient-derived organoids treated with JTE-607

Project description:To evaluate the impact of CPA inhibition on transcriptomic heterogeneity, we treated two lung cancer organoids and one liver cancer organoid with either DMSO or JTE-607, and subsequently pooled them for 3′ tag-based single-cell RNA sequencing using the 10x Genomics Chromium platform. For bioinformatic analysis, profiled cells were first demultiplexed and assigned to their respective organoids of origin based on expression and SNP profiles. We then quantified transcript abundance at polyadenylation site (PAS) resolution to generate a PAS-by-cell count matrix, allowing us to systematically investigate the effects of JTE-607 treatment on PAS usage patterns and cellular states.

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Project description:RNA-seq of dTAG-NUDT21 HCT116 cells treated with DMSO+JTE-607 or dTAGV1+JTE-607.

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scRNA-seq analysis of patient-derived organoids treated with JTE-607

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The anti-cancer compound JTE-607 reveals hidden sequence specificity of the mRNA 3' processing machinery

Project description:JTE-607 is a small molecule compound with anti-inflammation and anti-cancer activities. Upon entering the cell, it is hydrolyzed to Compound 2, which directly binds to and inhibits CPSF73, the endonuclease for the cleavage step in pre-mRNA 3' processing. Although CPSF73 is universally required for mRNA 3' end formation, we have unexpectedly found that Compound 2-mediated inhibition of pre-mRNA 3' processing is sequence-specific and that the sequences flanking the cleavage site (CS) are a major determinant for drug sensitivity. By using massively parallel in vitro assays, we have measured the Compound 2 sensitivities of over 260,000 sequence variants and identified key sequence features that determine drug sensitivity. A machine learning model trained on these data can predict the impact of JTE-607 on poly(A) site (PAS) selection and transcription termination genome-wide. We propose a biochemical model in which CPSF73 and other mRNA 3' processing factors bind to RNA of the CS region in a sequence-specific manner and the affinity of such interaction determines the Compound 2 sensitivity of a PAS. Together, our study not only characterized the mechanism of action of a compound with clinical implications, but also revealed a previously unknown sequence-specificity of the mRNA 3' processing machinery.

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Project description:Cleavage and polyadenylation (CPA) defines the 3’ end of almost all eukaryotic mRNAs. CPA inhibition, or CPAi, leads to transcriptional readthrough. Here, we show that the CPSF-73 inhibitor JTE-607 globally perturbs gene expression, especially for those with a high GC content and located in high gene density regions. Based on regulated alternative polyadenylation (APA) events, we found that more frequently used CPA sites are inhibited by JTE-607 to a greater extent. Consistently, cells with elevated CPA activities, as indicated by preferential usage of proximal APA sites, display greater transcriptional readthrough and gene expression disturbance upon JTE-607 treatment. Remarkably, overexpression of the core CPA factor FIP1 enhances global CPA activity in the cell and leads to greater JTE-607 sensitivity. Taken together, our data indicate that CPAi selectively impacts genes based on their genomic features and the CPA activity of a cell is a key determinant of sensitivity to CPAi.

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