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Expression Analysis of Mouse Tumor and Metastatic Pancreatic Ductal Adenocarcinoma Organoids

ABSTRACT: This study used Illumina strand-specific, paired-end RNA-sequencing to examine gene expression differences between matched murine tumor- and metastasis-derived mouse pancreatic ductal adenocarcinoma (PDAC) cells grown as three-dimensional, organoid cultures. The study analyzed 16 organoid lines derived from matched primary PDAC tumors and PDAC metastases from 6 KPC (KrasLSL-G12D; Trp53LSL-R172H; Pdx1-Cre) mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE142467 | GEO | 2020/06/16

REPOSITORIES: GEO

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Single-cell analysis of murine pancreatic ductal adenocarcinoma cells reveals the transcriptional dynamics of pancreatic cancer progression..

Project description:This study used 10X Genomics, single-cell RNA-sequencing to examine the differentiation states of cancer cells present in tumors derived from the KrasLSL-G12D; Trp53LSL-R172H; Pdx1-Cre (KPC) mouse model of pancreatic ductal adenocarcinoma. The study analyzed tumors from 8 different mice.

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Project description:This study used Illumina strand-specific, paired-end RNA-sequencing to examine gene expression differences between normal and neoplastic mouse pancreatic ductal cells grown as three-dimensional, organoid cultures. The study analyzed 19 independently derived organoid lines. These 19 lines included 7 biological replicate "mN," or mouse normal, organoid lines, derived from the pancreatic ductal cells of wild-type C57Bl/6J or C57Bl/6N mice. In addition, the study analyzed 6 biological replicate "mP," or mouse PanIN, organoid lines, derived from PanIN-containing mouse pancreata from the KrasLSL-G12D; Pdx1-Cre mouse model. (The presence of PanIN in the pancreata from which these organoid lines were derived was confirmed by examining histological sections from the same pancreata). The final 6 lines examined in this study were biological replicate "mT," or mouse tumor, organoid lines, derived from mouse pancreata containing pancreatic ductal adenocarcinoma (PDAC) from the KrasLSL-G12D; Trp53LSL-R162H; Pdx1-Cre mouse model. We genes differentially expressed in the PanIN- or tumor-derived mouse organoid lines, relative to the mouse normal organoids, that may reflect expression changes required for pancreatic tumorigenesis.

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Mechanisms of resistance to oncogenic KRAS inhibition in pancreatic cancer

Project description:KRAS inhibitors demonstrate clinical efficacy in pancreatic ductal adenocarcinoma (PDAC); however, resistance is common. Among patients with KRASG12C-mutant PDAC treated with adagrasib or sotorasib, mutations in PIK3CA and KRAS, and amplifications of KRASG12C, MYC, MET, EGFR, and CDK6 emerged at acquired resistance. In PDAC cell lines and organoid models treated with the KRASG12D inhibitor MRTX1133, epithelial-to-mesenchymal transition and PI3K-AKT-mTOR signaling associate with resistance to therapy. MRTX1133 treatment of the KrasLSL-G12D/+;Trp53LSL-R172H/+;p48-Cre (KPC) mouse model yielded deep tumor regressions, but drug resistance ultimately emerged, accompanied by amplifications of Kras, Yap1, Myc, and Cdk6/Abcb1a/b, and co-evolution of drug-resistant transcriptional programs. Moreover, in KPC and PDX models, mesenchymal and basal-like cell states displayed increased response to KRAS inhibition compared to the classical state. Combination treatment with KRASG12D inhibition and chemotherapy significantly improved tumor control in PDAC mouse models. Collectively, these data elucidate co-evolving resistance mechanisms to KRAS inhibition and support multiple combination therapy strategies.

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Mechanisms of resistance to oncogenic KRAS inhibition in pancreatic cancer

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Enhancer activation during tumor progression in the KrasLSLG12D/+; Trp53LSLR172H/+; Pdx1-Cre (KPC) mouse model of pancreatic ductal adenocarcinoma.

Project description:Murine pancreatic ductal adenocarcinoma tumor organoids (T6 and T23) were generated from primary tumors from KrasLSL-G12D/+; Trp53LSL-R172H/+; Pdx1-Cre mice. At the first passage, cells in Matrigel were overlaid with mouse complete medium alone or supplemented with 10 uM Nutlin-3a to select for cells that have undergone loss-of-heterozygosity (LOH) for the wild-type (wt, "+") allele of Trp53. Organoids were cultured for 3 passages in the presence or absense of Nutlin-3a, and then culturing was continued in unsupplemented mouse complete medium. H3K27ac ChIP-sequencing (ChIP-seq) was performed to identify regions differentially enriched for H3K27ac binding in Trp53-LOH vs. wt tumor organoids.

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RNA-seq single cells analysis of 2 tumors from KPC (KrasLSL-G12D/+ Trp53LSL-R172H/+ Pdx1-Cre) mice

Project description:RNA-seq single cells analysis of 2 tumors from KPC (KrasLSL-G12D/+ Trp53LSL-R172H/+ Pdx1-Cre) mice

| PRJNA471312 | ENA

Gene expression analysis between the pancreatic tissues of Pdx1-cre;Kras LSL-G12D and Pdx-cre;KrasLSL-G12D;IKK2/beta F/F mice

Project description:Constitutive Kras and NF-kB activation is identified as signature alterations in human pancreatic ductal adenocarcinoma (PDAC). Here, we report that pancreas-targeted IKK2/beta inactivation inhibited NF-kB activation and completely suppressed PDAC development. Our findings demonstrated that NF-kB is required for development of pancreatic ductal adenocarcinoma that was initiated by Kras activation. Pancreatic tissue from 4 groups of mice were used in this project: (1) the pancreas normal appearance of Pdx1-cre;KrasLSL-G12D;IKK2/beta mice, (2) the normal pancreas of Pdx1-cre;KrasLSL-G12D mice, (3) the pancreatic lesion of pancreatic intraepithelial neoplasia (PanIN) of Pdx1-cre;KrasLSL-G12D mice, and (4) the pancreatic lesion of PDAC of Pdx1-cre;KrasLSL-G12D mice. Each group included three mice. RNA samples from mouse pancreas were hybridized on GeneChip Mouse Gene 1.0 ST arrays (Affymetrix). Group (1) and group (2) were compared, and group (2), group (3) and group (4) were compared.

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