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Arid1a promotes tumor initiation but restrains progression and metastasis in liver cancer

ABSTRACT: Arid1a promotes tumor initiation but restrains progression and metastasis in liver cancer

PROVIDER: PRJNA377344 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5297830.fastq.gz	Fastqsanger.gz
	SRR5297850.fastq.gz	Fastqsanger.gz
	SRR5297860.fastq.gz	Fastqsanger.gz
	SRR5297870.fastq.gz	Fastqsanger.gz
	SRR5297831.fastq.gz	Fastqsanger.gz

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Arid1a promotes tumor initiation but restrains progression and metastasis in liver cancer [RNA-seq]

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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 promotes tumor initiation but restrains progression and metastasis in liver cancer

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