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ARID1A deficiency promotes pancreatic tumorigenesis by reducing KRAS-induced senescence

ABSTRACT: ARID1A deficiency promotes pancreatic tumorigenesis by reducing KRAS-induced senescence

PROVIDER: PRJNA673200 | ENA |

REPOSITORIES: ENA

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ARID1A deficiency promotes pancreatic tumorigenesis by reducing KRAS-induced senescence (ATAC-Seq)

Project description:ARID1A is one of the most frequently mutated epigenetic regulators in a wide spectrum of cancers. In this study, we identified the anti-senescence effect of ARID1A deficiency in the progression of pancreatic intraepithelial neoplasia (PanIN) by profiling the transcriptome of individual PanINs in the mouse model. Interestingly, we found that ARID1A deficiency activates the transcription of Aldehyde dehydrogenase 1 family, member A1 (ALDH1A1), which play essential roles in attenuating the senescence by significantly reducing reactive oxygen species (ROS) induced by oncogenic KRAS. Our findings further suggest that ALDH could be considered as a potential adjuvant target for prevention and treatment of pancreatic cancer.

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ARID1A deficiency promotes pancreatic tumorigenesis by reducing KRAS-induced senescence (ATAC-Seq)

Project description:ARID1A deficiency promotes pancreatic tumorigenesis by reducing KRAS-induced senescence (ATAC-Seq)

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ARID1A deficiency promotes pancreatic tumorigenesis by reducing KRAS-induced senescence (RNA-Seq I)

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ARID1A deficiency promotes pancreatic tumorigenesis by reducing KRAS-induced senescence

Project description:This SuperSeries is composed of the SubSeries listed below.

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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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