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Differentially expressed genes in KPC Cxcr2 KO vs KPC mouse PDAC

ABSTRACT: Differentially expressed genes in KPC Cxcr2 KO vs KPC mouse PDAC

PROVIDER: PRJEB13592 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1361620_1.fastq.gz	Fastqsanger.gz
	ERR1361620_2.fastq.gz	Fastqsanger.gz
	ERR1361621_1.fastq.gz	Fastqsanger.gz
	ERR1361621_2.fastq.gz	Fastqsanger.gz
	ERR1361622_1.fastq.gz	Fastqsanger.gz

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Differentially expressed genes in KPC Cxcr2 KO vs KPC mouse PDAC

Project description:Recently, Bailey et al (2016, Nature) defined four subtypes of pancreatic cancer that are associated with distinct histopathological characteristics and differential survival, namely, Squamous, Pancreatic Progenitor, Immunogenic, and ADEX (Aberrantly Differentiated Endocrine eXocrine). We set out to assess by RNASeq whether loss of CXCR2 was significantly associated with a specific PDAC subtype. Pancreatic tumors were harvested from KPC or KPC Cxcr2-/- mice at endpoint (n=5 v 5), RNA prepared, and RNASeq analysis carried out. Reads were analysed using the bcbio-nextgen framework (https://bcbio-nextgen.readthedocs.org/en/latest/). After quality control and adaptor trimming, reads were aligned to the mouse genome build (UCSC mouse mm10) using STAR. Counts for known genes were generated using the function featureCounts in the R/Bioconductor package \Rsubread\. The R/Bioconductor package edgeR was used to identify differentially expressed genes.

2018-03-31 | E-MTAB-4659 | biostudies-arrayexpress

RNA-seq to investigate differentially expressed genes in KPC mouse PDAC treated with CSF-1R small molecule inhibitor AZD7507 and/or the CXCR2 small molecule inhibitor AZD5069

Project description:Recently, we defined four subtypes of pancreatic cancer that are associated with distinct histopathological characteristics and differential survival, namely, Squamous, Pancreatic Progenitor, Immunogenic, and ADEX (Bailey et al 2016, Nature). We also found that loss of CXCR2 was associated with a switch away from the squamous subtype (Steele et al 2016, Cancer Cell). Here we set out to investigate whether inhibition of CSF1R could also result in an alteration of transcriptomic subtype. Pancreatic tumors were harvested from control KPC mice, or mice treated with CSF1R inhibitor (AZD7507) and/or CXCR2 inhibitor (AZD5069) (n≥5). Tissues were stored in RNAl8r at -80C before RNA was prepared, and RNASeq analysis carried out. Reads were analysed using the bcbio-nextgen framework (https://bcbio-nextgen.readthedocs.org/en/latest/). After quality control and adaptor trimming, reads were aligned to the mouse genome build (UCSC mouse mm10) using STAR. Counts for known genes were generated using the function featureCounts in the R/Bioconductor package Rsubread. The R/Bioconductor package edgeR was used to identify differentially expressed genes.

2018-05-01 | E-MTAB-6620 | biostudies-arrayexpress

RNA-seq of sorted KPC Sf3b1-K700E murine PDAC cells

Project description:We established a mouse model of KrasG12D, Trp53-/- and Sf3b1-K700E murine pancreatic cancer to elucidate the impact of the SF3B1 mutation found in human PDAC on the KPC mouse model.

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RNA-seq of epithelial cells flow-sorted from PDAC tumors derived from the orthotopic transplantation of PDAC T-LOH KPC organoids with either Egfr WT PSCs or Egfr KO PSCs in NSG mice

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Project description:the genetic inactivation of Khk-C enhanced the survival of KPC-driven PDAC model even in absence of high fructose diet. Moreover Khk-C knock out decreased the viability of KPC organoids and cancer cells, the migratory capability of PDAC cells in vitro and the growth of KPC cells in vivo in a cell autonomous manner.

2023-07-07 | E-MTAB-12746 | biostudies-arrayexpress

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Project description:RNA-seq to investigate differentially expressed genes in KPC mouse PDAC treated with CSF-1R small molecule inhibitor AZD7507 and or the CXCR2 small molecule inhibitor AZD5069

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Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy that resists current treatments. To test epigenetic therapy against this cancer we used the DNA demethylating drug 5-aza-2’-deoxycytidine (DAC) in a KrasLSL-G12D; p53LSL-R270H/+; Pdx1-cre; Brca1flex2/flex2 (KPC-Brca1) mouse model of aggressive stroma-rich PDAC. In untreated tumors, we found globally decreased 5-methyl-cytosine (5mC) in malignant epithelial cells and in cancer-associated myofibroblasts (CAFs), and increased amounts of 5-hydroxymethyl-cytosine (5HmC) in CAFs, in progression from pancreatic intraepithelial neoplasia (PanIN) to PDAC. DAC further reduced DNA methylation and slowed PDAC progression, markedly extending survival in an early treatment protocol and significantly though transiently inhibiting tumor growth when initiated later, without adverse side effects. Escaping tumors contained areas of sarcomatoid transformation with disappearance of CAFs. Mixing-allografting experiments and proliferation indices showed that DAC efficacy was due to inhibition of both the malignant epithelial cells and the stromal CAFs. Expression profiling and immunohistochemistry highlighted DAC-induction of STAT1 in the tumors, and DAC plus gamma-interferon produced an additive anti-proliferative effect on PDAC cells. DAC induced strong expression of the testis antigen DAZL in CAFs. These data show that DAC is effective against PDAC in vivo and provide a rationale for future studies combining hypomethylating agents with cytokines and immunotherapy. Treatment of a short-term explant culture of malignant epithelial cells from a KPC-Brca1 mouse pancreatic carcinoma, with 0.5 micromolar 5-aza-dC (decitabine; DAC) for 48 hours. The experiment includes 3 replicate plates untreated and 3 replicates treated.

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