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Synertistic effects of Arid1a inactivation and oncogenic Kras mutation on gene expression in mouse embryonic cells (MEFs)

ABSTRACT: Synertistic effects of Arid1a inactivation and oncogenic Kras mutation on gene expression in mouse embryonic cells (MEFs)

PROVIDER: PRJNA857645 | ENA |

REPOSITORIES: ENA

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Synertistic effects of Arid1a inactivation and oncogenic Kras mutation on gene expression in mouse embryonic cells (MEFs)

Project description:To explore transcriptomic mechanisms underlying the cooperative effect in the proliferative phenotype, we harvest MEFs of different genotypes (KA, K, A, WT) recombined and un-recombined. We performed RNA-seq analysis on 5 recombined (Ad-CMV-Cre) cell lines of each genotypic conditions (WT, Arid1a L/L , Kras-LSL-G12D, and Kras-LSL-G12D; Arid1a L/L) as well as 2 or 3 un-recombined (Ad-CMV-GFP) or mock-infected MEF cell lines.

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Synertistic effects of Arid1a inactivation and oncogenic Kras mutation on chromatin accessbility in mouse embryonic cells (MEFs)

Project description:Synertistic effects of Arid1a inactivation and oncogenic Kras mutation on chromatin accessbility in mouse embryonic cells (MEFs)

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Synergistic effects of Arid1a inactivation and oncogenic Kras mutation in mouse embryonic cells

Project description:Synergistic effects of Arid1a inactivation and oncogenic Kras mutation in mouse embryonic cells

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Synertistic effects of Arid1a inactivation and oncogenic Kras mutation on chromatin accessbility in mouse embryonic cells (MEFs)

Project description:To explore mechanisms underlying the cooperative effect in the proliferative phenotype, we harvest MEFs of different genotypes (KA, K, A, WT) recombined and un-recombined.

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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.

2018-07-03 | GSE114576 | GEO

Arid1a restrains Kras-dependent changes in acinar cell identity

2018-07-03 | GSE114567 | GEO

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.

2021-06-06 | GSE160440 | GEO

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

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

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Transcription profiling of human lung epithelial cells ollowing oncogenic KRAS expression and TBK1 suppression or infection with oncogenic KRAS (G12V) - SuperSeries

Project description:The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF- B anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. This SuperSeries is composed of the following subset Series:; GSE17643: Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression; GSE17671: Profiling of immortalized human lung epithelial cells following infection with oncogenic KRAS (G12V) Experiment Overall Design: Refer to individual Series

2009-10-31 | E-GEOD-17672 | biostudies-arrayexpress

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