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CPSF3 inhibition blocks pancreatic cancer cell proliferation through disruption of core histone mRNA processing

ABSTRACT: CPSF3 inhibition blocks pancreatic cancer cell proliferation through disruption of core histone mRNA processing

PROVIDER: PRJNA1061762 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27446500_1.fastq.gz	Fastqsanger.gz
	SRR27446500_2.fastq.gz	Fastqsanger.gz
	SRR27446501_1.fastq.gz	Fastqsanger.gz
	SRR27446501_2.fastq.gz	Fastqsanger.gz
	SRR27446502_1.fastq.gz	Fastqsanger.gz

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CPSF3 inhibition blocks pancreatic cancer cell proliferation through disruption of core histone mRNA processing

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with limited effective treatment options, potentiating the importance of uncovering novel drug targets. Here, we target Cleavage and Polyadenylation Specificity Factor 3 (CPSF3), the 3’ endonuclease that catalyzes mRNA cleavage during polyadenylation and histone mRNA processing. We find that CPSF3 is highly expressed in PDAC and is associated with poor prognosis. CPSF3 knockdown blocks PDAC cell proliferation and colony formation in vitro and tumor growth in vivo. Chemical inhibition of CPSF3 by the small molecule JTE-607 also attenuates PDAC cell proliferation and colony formation, while it has no effect on cell proliferation of non-transformed immortalized control pancreatic cells. Mechanistically, JTE-607 induces transcriptional read-through in replication-dependent histones, reduces core histone expression, destabilizes chromatin structure and arrests cells in the S-phase of the cell cycle. Therefore, CPSF3 represents a potential therapeutic target for the treatment of PDAC.

2024-01-06 | GSE252667 | GEO

CPSF3 inhibition blocks pancreatic cancer cell proliferation through disruption of core histone mRNA processing.

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with limited effective treatment options, potentiating the importance of uncovering novel drug targets. Here, we target cleavage and polyadenylation specificity factor 3 (CPSF3), the 3' endonuclease that catalyzes mRNA cleavage during polyadenylation and histone mRNA processing. We find that CPSF3 is highly expressed in PDAC and is associated with poor prognosis. CPSF3 knockdown blocks PDAC cell proliferation and colony formation in vitro and tumor growth in vivo. Chemical inhibition of CPSF3 by the small molecule JTE-607 also attenuates PDAC cell proliferation and colony formation, while it has no effect on cell proliferation of nontransformed immortalized control pancreatic cells. Mechanistically, JTE-607 induces transcriptional readthrough in replication-dependent histones, reduces core histone expression, destabilizes chromatin structure, and arrests cells in the S-phase of the cell cycle. Therefore, CPSF3 represents a potential therapeutic target for the treatment of PDAC.

| S-EPMC10870380 | biostudies-literature

Selective Disruption of Core Regulatory Transcription

Project description:Selective Disruption of Core Regulatory Transcription

| PRJNA494422 | ENA

Comprehensive investigation identifies CPSF3 as a novel prognostic and oncogenic biomarker in bladder cancer

Project description:Background Bladder cancer (BC) remains a prevalent malignancy worldwide, with rising incidence rates each year. Despite progress in therapeutic strategies, many patients suffer recurrence or progression, emphasizing the urgent need for novel prognostic biomarkers and therapeutic targets. This research evaluated the prognostic relevance and functional role of Cleavage and Polyadenylation Specificity Factor 3 (CPSF3) in BC. Methods We analyzed CPSF3 expression using The Cancer Genome Atlas data and immunohistochemistry on a cohort of 203 BC patients. A nomogram incorporating CPSF3 expression was developed based on CPSF3 expression for prediction of overall survival and disease-free survival. Immune infiltration analyses and transcriptome sequencing were performed to explore underlying biological mechanisms. In vitro and in vivo experiments were utilized to examine the results of CPSF3 silencing on bladder cancer cell growth, colony-forming ability and cell cycle transitions. Results Elevated CPSF3 expression was significantly linked to unfavorable overall survival and disease-free survival both in TCGA datasets and our cohort. The CPSF3-based nomogram outperformed conventional prognostic models. CPSF3 expression was associated with tumor-infiltrating immune cells and immune checkpoint markers. Enrichment analysis revealed CPSF3 enrichment in cell cycle-related pathways. Suppression of CPSF3 expression led to marked reductions in cell proliferation, colony formation, tumor growth in animal models and inhibited G1 to S phase progression. Conclusion CPSF3 is a promising prognostic biomarker for BC and may play a crucial role in BC progression. Incorporating CPSF3 into clinical prognostic models may enhance prediction of patient outcomes. CPSF3 may represent a promising therapeutic target for BC management.

2025-09-14 | GSE307514 | GEO

Selective Disruption of Core Regulatory Transcription [ChIP-seq]

Project description:Selective Disruption of Core Regulatory Transcription [ChIP-seq]

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Selective Disruption of Core Regulatory Transcription [AQuA-HiChIP]

Project description:Selective Disruption of Core Regulatory Transcription [AQuA-HiChIP]

| PRJNA494423 | ENA

Selective Disruption of Core Regulatory Transcription [RNA-seq]

Project description:Selective Disruption of Core Regulatory Transcription [RNA-seq]

| PRJNA495665 | ENA

Oxaboroles target trypanosome CPSF3

Project description:Oxaboroles target trypanosome CPSF3 - DDD85646 screen

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Oxaboroles target trypanosome CPSF3

Project description:Oxaboroles target trypanosome CPSF3 - SCYX-6759 screen

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ChIP-seq analysis for core 3' processing factors in control and U1 AMO-treated HeLa cells

Project description:To understand the effect of U1 AMO treatment on chromatin binding profiles of core 3' processing factors, we carried out ChIP-seq analysis for several core 3' processing factors after control and U1 AMO treatment

2023-02-27 | GSE193202 | GEO

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