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Bulk RNA-Seq comparing pancreatic acinar cells based on their expression levels of KRAS protein (Citrine-KRAS fusion)

ABSTRACT: Bulk RNA-Seq comparing pancreatic acinar cells based on their expression levels of KRAS protein (Citrine-KRAS fusion)

PROVIDER: PRJNA684492 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13242007_1.fastq.gz	Fastqsanger.gz
	SRR13242007_2.fastq.gz	Fastqsanger.gz
	SRR13242008_1.fastq.gz	Fastqsanger.gz
	SRR13242008_2.fastq.gz	Fastqsanger.gz
	SRR13242009_1.fastq.gz	Fastqsanger.gz

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Bulk RNA-Seq comparing pancreatic acinar cells based on their expression levels of KRAS protein (Citrine-KRAS fusion)

Project description:We developped new mouse models to detect endogenous KRAS protein expression pattern via a Citrine-KRAS (Cit-K) fusion construction

2021-05-01 | GSE163039 | GEO

Arid1a restrains Kras-dependent changes in acinar cell identity

Project description:Mutations in members of the SWI/SNF chromatin remodeling family are common events in human cancer, but the mechanisms whereby disruption of SWI/SNF components alters tumorigenesis remain poorly understood. To model the effect of loss of function mutations in the SWI/SNF subunit Arid1a in pancreatic ductal adenocarcinoma (PDAC) initiation, we directed shRNA triggered, inducible and reversible suppression of Arid1a to the pancreas of mice in the setting of oncogenic KrasG12D. Arid1a cooperates with Kras in the adult pancreas as postnatal silencing of Arid1a following sustained KrasG12D expression induces rapid and irreversible reprogramming of acinar cells into mucinous PDAC precursor lesions. In contrast, Arid1a silencing during embryogenesis, concurrent with KrasG12D activation, leads to retention of acinar cell fate. Together, our results demonstrate Arid1a as a critical modulator of Kras-dependent changes in acinar cell identity, and underscore an unanticipated influence of timing and genetic context on the effects of SWI/SNF complex alterations in epithelial tumorigenesis.

2018-07-03 | GSE114567 | GEO

Arid1a restrains Kras-dependent changes in acinar cell identity

2018-07-03 | GSE114576 | GEO

Arid1a restrains Kras-dependent changes in acinar cell identity

Project description:Arid1a restrains Kras-dependent changes in acinar cell identity

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Arid1a restrains Kras-dependent changes in acinar cell identity

Project description:Arid1a restrains Kras-dependent changes in acinar cell identity

| PRJNA471811 | ENA

RBPJ deficiency sensitizes pancreatic acinar cells to Kras-mediated PanIN initiation

Project description:Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis and is among the most common causes of cancer death worldwide. KrasG12D mutation is the main driver mutation but insuffi-cient for progression of invasive cancer on its own indicating that other pathways, such as Notch signaling may participate in that process. RBPJ, the only transcription factor in Notch signaling, is frequently lost in human cancers and associated with more aggressive breast cancer phenotype. Notch-independently, in complex with P48, RBPJ initiates transcription of its paralogue RBPJL ensuring acinar differentiation. The RBPJ knockout has an embryonic lethal effect. Mice with pancreas-specific deletion of RBPJ presented with less acinar tissue and large duct-like structures suggesting a relevance of RBPJ for acinar to ductal reprogramming and even pancreatic neoplasia. Here, we found reduced RBPJ expression level in the human PDAC specimens. Analyses of transgenic mouse models of an inducible P48-dependent RBPJ knockout revealed that it is dispensable for the maintenance adult acinar cells. In the context of oncogenic KRAS expression, the RBPJ deficiency facilitated the development of PanIN lesions with massive fibrotic stroma. Interestingly, RNA seq data revealed corresponding transcription pattern prior to phenotypic alterations.

2023-10-03 | GSE189756 | GEO

In vivo reprogramming drives Kras-induced cancer development [expression]

Project description:Accumulation of genetic mutations is thought to be a primary cause of cancer. However, a set of genetic mutations sufficient for cancer development remains unclear in most cancers, including pancreatic cancer. Here, we examined the effect of in vivo reprogramming on Kras-induced cancer development. We first demonstrate that Kras and p53 mutations are insufficient to induce activation of ERK signaling and cancer development in the pancreas. We next show that short transient expression of reprogramming factors (1-3 days) in pancreatic acinar cells results in repression of acinar cell enhancers and reversible loss of acinar cell properties. Notably, the transient expression of reprogramming factors in Kras mutant mice is sufficient to induce robust and persistent activation of ERK signaling in acinar cells and rapid formation of pancreatic ductal adenocarcinoma (PDAC). In contrast, forced expression of acinar cell-related transcription factors inhibits pancreatitis-induced activation of ERK signaling and development of precancerous lesions in Kras-mutated acinar cells.

2018-05-16 | GSE100840 | GEO

In vivo reprogramming drives Kras-induced cancer development [ChIP-seq]

2018-05-16 | GSE100841 | GEO

RNAseq data comparing iKPC PDAC tumors with KRAS* expression (ON) and KRAS extinction (OFF)

Project description:RNAseq data comparing iKPC PDAC tumors with KRAS* expression (ON) and KRAS extinction (OFF)

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RNAseq data comparing GFP, wildtype USP21 and enzyme-dead USP21 overexpressing iKPC PDAC cells with KRAS* expression (on dox) and KRAS* extinction (off dox)

Project description:USP21 promotes PDAC tumor cells to bypass KRAS* dependency. To dissect the molecular mechanism, we conducted RNA-seq analysis comparing iKPC cancer cells overexpressing GFP, wildtype USP21 and enzyme-dead USP21 at day 3 after KRAS* extinction. KRAS*-expressing iKPC cells with GFP overexpression are positive control.

2021-09-17 | GSE178860 | GEO

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