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Genome wide CRISPR/Cas9 screen identifies the coagulation factor IX (F9) as a regulator of senescence

ABSTRACT: Genome wide CRISPR/Cas9 screen identifies the coagulation factor IX (F9) as a regulator of senescence

PROVIDER: PRJNA791842 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17319712_1.fastq.gz	Fastqsanger.gz
	SRR17319712_2.fastq.gz	Fastqsanger.gz
	SRR17319713_1.fastq.gz	Fastqsanger.gz
	SRR17319713_2.fastq.gz	Fastqsanger.gz
	SRR17319714.fastq.gz	Fastqsanger.gz

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Genome wide CRISPR/Cas9 screen identifies the coagulation factor IX (F9) as a regulator of senescence

Project description:During this last decade the development of pro-senescence therapies has become an attractive strategy as cellular senescence acts as a barrier against tumour progression. In this context, CDK4/6 inhibitors induce senescence and reduce tumour growth in breast cancer patients. However, even though cancer cells are arrested after CDK4/6 inhibitor treatment, genes regulating senescence in this context are still unknown limiting their anti-tumour activity. Here, using a functional genome wide CRISPR/Cas9 genetic screen we found several genes that participate in the proliferation arrest induced by CDK4/6 inhibitors. We find that downregulation of the coagulation factor IX (F9) using sgRNA and shRNA prevents the cell cycle arrest and senescent-like phenotype induced in MCF7 breast tumour cells upon Palbociclib treatment. These results were confirmed using another breast cancer cell line, T47D, and with an alternative CDK4/6 inhibitor, Abemaciclib, and further tested in a panel of 22 cancer cells. While F9 knockout prevents the induction of senescence, treatment with a recombinant F9 protein was sufficient to induce a cell cycle arrest and senescence-like state in MCF7 tumour cells. Besides, endogenous F9 is upregulated in different human primary cells cultures undergoing senescence. Importantly, bioinformatics analysis of cancer datasets suggest a role for F9 in human tumours. Altogether, these data collectively propose key genes involved in CDK4/6 inhibitor response that will be useful to design new therapeutic strategies in personalized medicine in order to increase their efficiency, stratify patients and avoid drug resistance.

2022-03-31 | GSE192525 | GEO

Genome wide CRISPR/Cas9 screen identifies the coagulation factor IX (F9) as a regulator of senescence.

Project description:During this last decade, the development of prosenescence therapies has become an attractive strategy as cellular senescence acts as a barrier against tumour progression. In this context, CDK4/6 inhibitors induce senescence and reduce tumour growth in breast cancer patients. However, even though cancer cells are arrested after CDK4/6 inhibitor treatment, genes regulating senescence in this context are still unknown limiting their antitumour activity. Here, using a functional genome-wide CRISPR/Cas9 genetic screen we found several genes that participate in the proliferation arrest induced by CDK4/6 inhibitors. We find that downregulation of the coagulation factor IX (F9) using sgRNA and shRNA prevents the cell cycle arrest and senescent-like phenotype induced in MCF7 breast tumour cells upon Palbociclib treatment. These results were confirmed using another breast cancer cell line, T47D, and with an alternative CDK4/6 inhibitor, Abemaciclib, and further tested in a panel of 22 cancer cells. While F9 knockout prevents the induction of senescence, treatment with a recombinant F9 protein was sufficient to induce a cell cycle arrest and senescence-like state in MCF7 tumour cells. Besides, endogenous F9 is upregulated in different human primary cells cultures undergoing senescence. Importantly, bioinformatics analysis of cancer datasets suggest a role for F9 in human tumours. Altogether, these data collectively propose key genes involved in CDK4/6 inhibitor response that will be useful to design new therapeutic strategies in personalised medicine in order to increase their efficiency, stratify patients and avoid drug resistance.

| S-EPMC8858321 | biostudies-literature

De novo contiguous deletion of F9 and SOX3 genes on the X chromosome in a child with Haemophilia B and partial hypopituitarism

Project description:Case report of a child with Haemophilia B (factor IX deficiency), partial hypopituitarism, subtle dysmorphism and mild developmental delay, where a 2.31Mb de novo deletion of Xq27.1-q27.2 was identified on array CGH investigations (using a sample from a healthy, annoymous donor as control). This contiguous deletion includes the genes F9 and SOX3 and therefore provides a cause for this patient's abnormal phenotype.

2014-12-31 | E-MEXP-3782 | biostudies-arrayexpress

Klebsiella pneumoniae strain:F9 | isolate:F9

Project description:Klebsiella pneumoniae strain:F9 | isolate:F9 Genome sequencing and assembly

| PRJNA1018462 | ENA

A CpG mutational hotspot in a ONECUT (HNF6) binding site accounts for the prevalent variant of Hemophilia B Leyden

Project description:Hemophilia B, or the 'Royal Disease', arises from mutations in the Coagulation Factor IX (F9) gene. Mutations within the F9 promoter are associated with a remarkable form of the disease, termed Hemophilia B Leyden, in which symptoms ameliorate after puberty. Mutations at the -5/-6 site account for the majority of Leyden cases, and have been postulated to disrupt the binding of a transcriptional activator, the identity of which has remained elusive for more than twenty years. Here we show that the ONECUT transcription factors (ONECUT1/HNF6 and ONECUT2/HNF6B) bind to the -5/-6 site. The various Hemophilia B Leyden mutations that have been reported in this site inhibit ONECUT binding to varying degrees that correlate well with their associated clinical severities. In addition, expression of F9 is crucially dependent on ONECUT factors in vivo and as such, mice that are deficient in either ONECUT1, ONECUT2 or both, exhibit depleted levels of F9. Taken together, our findings establish the ONECUT transcription factors as the missing regulators of Hemophilia B Leyden that operate through the -5/-6 site.

2013-03-06 | E-MTAB-890 | biostudies-arrayexpress

Microarray screening of RARgamma responsive genes in F9 teratocarcinoma cells

Project description:We compared the differentially expressed genes between the F9 Wt cells and F9 RAR gamma knock out cells before and after RA treatment. 3 replicates for each conditions. We also identified the RA responsive genes in the F9 Wt cells. Keywords: mutant type

2007-12-18 | GSE8431 | GEO

F9 Embryonal Carcinoma cell line

Project description:Expression profile for undifferentiated F9 Embryonal Carcinoma cell line Keywords: expression profile

2008-02-27 | GSE10606 | GEO

Phf19 knockdown effect on F9 embryonal carcinoma cells

Project description:PCL family protein Phf19/Pcl3 is one of the accessory components of the PRC2 core complex, and Phf19 is highly expressed in murine ES cells and an ES cell-like embryonic carcinoma cell line, F9 cells. Here we performed microarray analysis of embryonal carcinoma cell line F9 following Phf19 knockdown by shRNA. Knocking down Phf19/Pcl3 in F9 embryonic cells led to derepression of numerous PRC2 direct target genes.

2012-12-20 | GSE42463 | GEO

Acinetobacter sp. F9 strain:F9 | isolate:camel feces

Project description:Acinetobacter sp. F9 strain:F9 | isolate:camel feces Genome sequencing

| PRJNA741472 | ENA

Gene expression in F9 teratocarcinoma cells

Project description:Dr. Esko's laboratory focuses on the structure, function, and biosynthesis of glycoproteins and proteoglycans. This laboratory also works on the design and synthesis of small molecule inhibitors of glycosylation. Gene expression in F9 teratocarcinoma cells: Study of the differential expression of glycosyltransferases, sulfotransferases and proteoglycan core proteins in F9 teratocarcinoma cells before and after differentiation with retinoic acid/theophylline/cAMP. Published data indicated that differentiation of the cells induces the synthesis of anticoagulant heparin-like compounds and a large increase in overall glycosaminoglycan synthesis.

2011-03-02 | GSE27592 | GEO

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