Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Multi-omic profiling of lung and liver tumor microenvironments of metastatic pancreatic cancer reveals site-specific immune-regulatory features [RNA-seq]

ABSTRACT: To understand the site-specific differences in how metastatic pancreatic cancer is modulated, we compared the non-immune compartments by bulk RNA-seq by mouse models of lung and liver metastatic pancreatic cancer based on Kras and Trp53 driven pancreatic cancer cells (KPC).

ORGANISM(S): Mus musculus

PROVIDER: GSE172104 | GEO | 2021/04/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Multi-omic profiling of lung and liver tumor microenvironments of metastatic pancreatic cancer reveals site-specific immune-regulatory pathways [WES]

Project description:WES was used to analyze the mutational landscape of KPC and Panc02, two murine pancreatic cancer cell lines. As expected, a relatively low mutational burden was identified in KPC cells.

2021-04-15 | GSE172105 | GEO

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.

2022-06-07 | GSE203339 | GEO

Mesothelin secretion by pancreatic cancer cells co-opts macrophages and promotes metastasis

Project description:SILAC-based proteomic analysis was performed on the secretome of the low metastatic FC1199 and high metastatic FC1245 KPC derived pancreatic cancer cell lines in order to identify secreted proteins that correlate with increased metastasis.

2023-12-19 | PXD042234 | Pride

Muscle and adipose transcriptome in a mouse model of cachexia induced by orthotopic pancreatic cancer, with and without tumor-derived interleukin-6 (IL-6)

Project description:Pancreatic ductal adenocarcinoma (PDAC) causes involuntary wasting of adipose and muscle tissue, also known as cachexia. Cachexia is a major cause of cancer-related deaths, particularly among patients with PDAC. Here we profiled gene expression in adipose tissue and skeletal muscle in normal/sham control mice and in mice bearing orthotopic PDAC tumors. PDAC tumors were initiated by intra-pancreatic injection of a cell line derived from the KPC (Kras-G12D;Trp-R172H;Pdx1::Cre) genetically engineered mouse model of pancreatic cancer, or by injection of the same cell line deleted for the IL6 gene using CRISPR/Cas9. KPC-IL6 knockout (ko) cells caused less adipose wasting and no muscle loss compared with KPC-wildtype (wt) cells.

2021-04-07 | GSE123310 | GEO

Multi-omic profiling of lung and liver tumor microenvironments of metastatic pancreatic cancer reveals site-specific immune-regulatory features

Project description:Multi-omic profiling of lung and liver tumor microenvironments of metastatic pancreatic cancer reveals site-specific immune-regulatory features

| PRJNA722014 | ENA

ZDHHC20-Mediated S-Palmitoylation of YTHDF3 Stabilizes MYC mRNA to Promote Pancreatic Cancer Progression

Project description:Post-translational modifications of malignant transformation and tumor maintenance in pancreatic ductal adenocarcinoma (PDAC) in the context of KRAS signaling remains largely unexplored. Here, we used the KPC mouse model to examine the effect of palmitoylation on pancreatic cancer progression. ZDHHC20, upregulated by KRAS, is abnormally overexpressed and associated with poor prognosis in patients with pancreatic cancer. Dysregulation of ZDHHC20 promotes pancreatic cancer progression in a palmitoylation-dependent manner. ZDHHC20 inhibits lysosomal localization and degradation of YTHDF3 through S-palmitoylation of Cys474, which can result in abnormal accumulation of the oncogenic product MYC and thereby promote the malignant phenotypes of cancer cells. Further, we designed a biologically active YTHDF3-derived peptide to competitively inhibit YTHDF3 palmitoylation mediated by ZDHHC20, which in turn downregulated MYC expression and inhibited the progression of KRAS mutant pancreatic cancer. Thus, these findings highlight the therapeutic potential of targeting the ZDHHC20-YTHDF3-MYC signaling axis in pancreatic cancer.

2024-04-22 | GSE235516 | GEO

Multi-omic profiling of lung and liver tumor microenvironments of metastatic pancreatic cancer reveals site-specific immune-regulatory features [RNA-seq]

Project description:Multi-omic profiling of lung and liver tumor microenvironments of metastatic pancreatic cancer reveals site-specific immune-regulatory features [RNA-seq]

| PRJNA722017 | ENA

Wild Type Tumor Repressor Protein 53 (TRP53) Promotes Ovarian Cancer Cell survival

Project description:Loss of Pten in the KrasG12D;Amhr2-Cre mutant mice leads to the transformation of ovarian surface epithelial (OSE) cells and rapid development of low-grade, invasive serous adenocarcinomas. Tumors occur with 100% penetrance and express elevated expression of wild type tumor repressor protein 53 (TRP53). To test the functions of TRP53 in the Pten;Kras (Trp53+) mice, we disrupted the Trp53 gene yielding Pten;Kras(Trp53-) mice. By comparing morphology and gene expression profiles in the Trp53+ and Trp53- OSE cells, we document that wild-type TRP53 acts as a major promoter of OSE cell survival and differentiation: cells lacking Trp53 are transformed yet are less adherent, migratory and invasive and exhibit a gene expression profile more like normal OSE cells. These results provide a new paradigm: wild type TRP53 does not preferentially induce apoptotic or senescent related genes in the Pten;Kras(Trp53+) cancer cells but rather increases genes regulating DNA repair, cell cycle progression and proliferation and decreases putative tumor suppressor genes. However, if TRP53 activity is forced higher by exposure to nutlin-3a (an MDM2 antagonist), TRP53 suppresses DNA repair genes and induces the expression of genes that control cell cycle arrest and apoptosis. Thus, in the Pten;Kras(Trp53+) mutant mouse OSE cells and likely in human TP53+ low grade ovarian cancer cells, wild type TRP53 controls global molecular changes that are dependent on its activation status. These results suggest that activation of TP53 may provide a promising new therapy for managing type I ovarian cancer and other cancers in humans where wild-type TP53 is expressed. A direct comparison of ovarian surface epithelia cells from three different genotype mice

2012-06-20 | E-GEOD-34882 | biostudies-arrayexpress

RNAi off-target analysis in Trp53-/- mouse embryonic fibroblasts transduced with miRNA-based shRNAs targeting Trp53.

Project description:We analyzed miRNA-based shRNA off-target effects by transducing Trp53-/- MEFs at single- and high-copy with six well-characterized, potent and weak Trp53 shRNAs. To advance RNAi therapy for KRAS-mutant cancer, we developed a functionally validated library of siRNAs against RAS pathway genes that minimize off-target effects and enable combination gene silencing at low dose. We developed an in vivo model for real-time tracking of nanoparticle-based siRNA delivery and offer proof-of-principle that siRNA-mediated inhibition of a single gene (KRAS) or combinations of genes (A/B/C-RAF or KRAS+PIK3C-A/B) can impair the growth of KRAS-mutant colorectal cancer xenografts. Trp53-/- MEFs were transduced with LMP expressing Trp53 shRNAs at single copy (11-21% infection efficiency) and high copy (>98% infection efficiency), selected on puromycin and grown in absence of the selection agent before harvest. Uninfected Trp53-/- MEFs and Trp53-/- MEFs infected with an empty vector control served as M-bM-^@M-^\no shRNAM-bM-^@M-^] reference.

2014-08-01 | E-GEOD-59952 | biostudies-arrayexpress

Gene expression profiling of mouse pancreatic tumors derived from acinar or ductal cells

Project description:Acinar and ductal cells are the major epithelial cell types in the exocrine pancreas, but which of these serves as the cell-of-origin in human PDAC has been debated. Our mouse models have demonstrated that oncogenic Kras expression and Trp53 loss in pancreatic acinar or ductal cells can lead to pancreatic cancer. Here, we performed gene expression profiling of bulk acinar cell-derived and ductal cell-derived mouse pancreatic tumors to identify the transcriptomic profiles.

2021-01-05 | GSE164180 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data