Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile at single cell level of macrophages in PDAC liver metastasis

ABSTRACT: We used single cell RNA sequencing to investigate macrophage heterogeneity and their temporal and spatial distributions in PDAC liver metastasis

ORGANISM(S): Mus musculus

PROVIDER: GSE215118 | GEO | 2023/12/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profile at single cell level of macrophages in PDAC liver metastasis

Project description:Gene expression profile at single cell level of macrophages in PDAC liver metastasis

| PRJNA888802 | ENA

Truncated O-glycan connection to Cancer: Depletion of O-glycosyltransferase C1GALT1 leads to early PDAC onset and metastasis

Project description:Aberrant expression of truncated O-glycan structures, such as Tn and STn, is frequently observed in pancreatic ductal adenocarcinoma (PDAC). The focus of our study is to investigate the functional role of truncated O-glycans in PDAC progression and metastasis. Our study revealed that kmockout of C1GALT1 leads to increased expression of truncated glycans and accelerates PDAC progression and metastasis.

2018-10-05 | GSE104607 | GEO

Single cell gene expression profile of tumor-associated fibroblasts from macrophage-depleted PDAC liver metastasis

Project description:We used single cell RNA sequencing to investigate how macrophages regulate tumor-associated fibroblast heterogeneity in PDAC liver metastasis

2024-04-04 | GSE232335 | GEO

IL-1b+ tumor-associated macrophages fuel pathogenic inflammation in pancreatic cancer - scRNAseq of human PDAC samples

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with high resistance to therapy. Inflammatory and immunomodulatory signals co-exist in the tumor microenvironment (TME), leading to dysregulated reparative and cytotoxic responses. Tumor-associated macrophages (TAMs) control immune dynamics in the TME, but their heterogeneity and plasticity have hampered understanding of the underlying mechanisms. Here, we combined single-cell and spatial genomics with functional experiments to elucidate macrophage functions in PDAC. We uncovered an inflammatory loop between tumor cells and interleukin (IL)-1b+ TAMs, a subset of macrophages elicited by a local synergy between prostaglandin E2 (PGE2) and tumor necrosis factor (TNF)-a. Interfering with the PGE2-IL-1b axis elicited TAM reprogramming and antagonized tumor-intrinsic inflammation, leading to PDAC control in vivo. IL-1b+ TAMs are conserved across human cancers and correlate with inflammation and patient prognosis in a context-dependent manner. Our study highlights how TAMs govern between inflammation and immune suppression in cancer, with significant therapeutic implications.

2023-09-11 | GSE217845 | GEO

IL-1b+ tumor-associated macrophages fuel pathogenic inflammation in pancreatic cancer - scRNA-seq of murine PDAC samples

2023-09-11 | GSE217846 | GEO

IL-1b+ tumor-associated macrophages fuel pathogenic inflammation in pancreatic cancer - Spatial transcriptomics of mouse PDAC samples

2023-09-11 | GSE217843 | GEO

IL-1b+ tumor-associated macrophages fuel pathogenic inflammation in pancreatic cancer - Molecular Cartography of human PDAC samples

2023-09-11 | GSE237846 | GEO

Single cell gene expression profile of tumor-associated fibroblasts from macrophage-depleted PDAC liver metastasis

Project description:Single cell gene expression profile of tumor-associated fibroblasts from macrophage-depleted PDAC liver metastasis

| PRJNA971635 | ENA

ShRNA screen identifies novel mediator of PDAC metastasis in vivo

Project description:ShRNA screen identifies novel mediator of PDAC metastasis in vivo

| PRJNA926988 | ENA

The role of KLF7 in pancreatic adenocarcinoma (PDAC) progression

Project description:Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with a dismal prognosis. Currently, there is no effective therapy to treat PDAC, and thus detailed molecular and functional evaluation of PDAC is needed to identify and develop better therapeutic strategies. Here we show that the transcription factor Kruppel-like factor 7 (KLF7) is overexpressed in PDAC and that inhibition of KLF7 blocks PDAC tumor growth and metastasis in cell culture and in mice. KLF7 expression in PDAC can be upregulated due to activation of a MAP kinase pathway or inactivation of the tumor suppressor p53, two alterations that occur in a large majority of PDACs. ShRNA-mediated knockdown of KLF7 inhibits the expression of interferon-stimulated genes (ISGs), which are necessary for KLF7-mediated PDAC tumor growth and metastasis. KLF7 knockdown also results in the downregulation of Discs Large MAGUK Scaffold Protein 3 (DLG3), resulting in Golgi complex fragmentation, and reduced protein glycosylation leading to reduced secretion of cancer-promoting growth factors such as chemokines. Genetic or pharmacological activation of Golgi complex fragmentation blocks PDAC growth and metastasis similar to KLF7 inhibition. Our results demonstrate a therapeutically amenable, KLF7-driven pathway that promotes PDAC growth and metastasis by activating ISGs and maintaining Golgi complex integrity.

2020-04-16 | GSE107184 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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