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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

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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.

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Arid1a restrains Kras-dependent changes in acinar cell identity

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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.

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