Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA257164 | ENA |
REPOSITORIES: ENA
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Project description:tumor-stroma crosstalk drives pancreatic carcinogenesis we used time-resolved genome-wide transcriptional profiling to analyse changes caused by co-exposure of pancreatic tumor and stellate cells Primary pancreatic Stellate cells (PSC) were treated with a cumulative supernatant of pancreatic tumor cell lines (n=8) and harvested at 1-7, and 24 hours post exposure for RNA extraction and hybridization on Affymetrix microarrays. The 8 tumor cell lines are pancreatic ductal adenocarcinoma lines: AsPC1, BxPC3, Capan1, Colo357, MiaPaca2, Panc1, Su8686, and T3M4
2013-08-09 | E-GEOD-49583 | biostudies-arrayexpress
Project description:Bulk RNAseq of pancreatic stellate cells (PSC) treated with DMXAA, interferon gamma or DMSO control. PSC were cultured alone as mono-cultures or in co-culture with mouse tumour organoids, The PSC were recovered by FACS using fluorecent protein mKate-2.
2025-03-19 | E-MTAB-14943 | biostudies-arrayexpress
Project description:It has been reported that lactate plays as a bridging signaling molecule to coordinates tumor cell and tumor stroma. As pancreatic stellate cells (PSC) is the most majority and functional cells in tumor microenvironment (TME) of pancreatic cancer (PC), whether the lactate involving the crosstalk between PSC and pancreatic acinar cells (PACs) in tumorigenesis of PC has not been defined. The present study showed that lactate transporter, monocarboxylate transporter 1 (MCT1) was predominantly expressed in pancreatic stellate cells (PSC), and correlates with worse prognosis in PC patients. Moreover, we revealed lactate induced autophagy-mediated activation of PSC, while knockout MCT1 in PSC (PSC-MCT1-/- mice) obviously inhibited the proliferation and metastasis of PC in vivo. Meanwhile, results of single-cell sequence demonstrated that the PD-1 expression in CD8+T cells was dramatically increased. Mechanistically, the MCT1-mediated influx of lactate activated PSC by inducing lactylation of lysine residues K356 and K781 on Vps34, a key regulator for autophagy. Moreover, the PSC-derived CXCL9/CXCL10 upregulated PD-1 expression via activating CXCR3/STAT3 pathway in CD8+ T. Consistently, the growth of pancreatic tumor in situ was significantly inhibited in mice treated with MCT1 inhibitor AZD3965, which was further suppressed by combination with PD-1 antibody. In conclusion, our study implicates lactate functions as TME transducer mediating activation of PSC and formation of immunosuppressive TME, and indicates the synergistic effect of targeting PSC activation in immune checkpoint therapy in PC.
2025-04-30 | GSE293004 | GEO
Project description:Bulk RNAseq of pancreatic stellate cells (PSC) and tumour cells treated with STING agonist DMXAA, STING inhibitor H151 or DMSO control. PSC were cultured alone as mono-cultures or in co-culture with mouse tumour organoids, The PSC and tumour cells were recovered by FACS using fluorecent proteins mKate-2 and tGFP, respectively.
2025-03-19 | E-MTAB-14946 | biostudies-arrayexpress
Project description:Bone marrow-derived mouse neutrophils were cultured in vitro in conditioned media from pancreatic stellate cell (PSC) cultures where the PSCs were treated with the STING agonist DMXAA or vehicle control to induce an ifCAF phenotype.
2025-03-18 | E-MTAB-14934 | biostudies-arrayexpress
Project description:The goal of this experiment is to characterize the different cancer associated CAF subtypes that can be induced by tumour-derived signlas in pancreatic stellate cells (PSC). Co-cultures of PSC and tumour organoids were seeded in matrigel and grown for 6 days in basal media. Mono-cultures of PSC were used as controls. The PSCs were recovered by flow cytometry and subjected to single cell RNA-seq profiling via the ddSeq-Surecell system.
2025-03-21 | E-MTAB-14944 | biostudies-arrayexpress
Project description:The goal of this experiment is to characterize the differentiation trajectories of pancreatic stellate cells (PSC) exposed to tumour-derived signals over a 6 days time series. Co-cultures of PSC and tumour organoids were seeded in matrigel and grown for 0-6 days in basal media. Mono-cultures of PSC were used as controls. The PSCs were recovered by flow cytometry at successive time points and subjected to single cell RNA-seq profiling via the ddSeq-Surecell system.
2025-03-21 | E-MTAB-14945 | biostudies-arrayexpress
Project description:Pancreatic stellate cells (PSCs) are components of normal pancreatic mesenchyme, and give rise to cancer-associated fibroblasts during pancreatic tumorigenesis. We used single cell RNA sequencing (scRNA-seq) to analyze PSCs and PSC-derived CAFs from normal pancreas and pancreatic cancer tissues, respectively.
2024-09-30 | GSE278162 | GEO
Project description:In pancreatic ductal adenocarcinoma (PDAC), differentiation of pancreatic stellate cells (PSCs) into myofibroblast-like cancer-associated fibroblasts (CAFs) promotes fibrotic, therapy-resistant tumours. Conversely, suppression of CAFs can result in aggressive metastatic tumours. Here we show that the Rho-effector kinase protein kinase N2 (PKN2) is critical for PSC myofibroblast differentiation. Loss of PKN2 was associated with reduced PSC proliferation and contractility, retention of lipid droplets and decreased a-SMA stress fibres. PKN2 loss was also associated with a myofibroblast CAF to -like inflammatory CAF switch in the PSC matrisome signature both in vitro and in vivo. In spheroid co-cultures with PDAC cells, loss of PKN2 prevented PSC invasion but, counter-intuitively, promoted invasive cancer cell outgrowth. Further, deletion of PKN2 in the pancreatic stroma induced more locally invasive, orthotopic pancreatic tumours. Finally, we demonstrated that a PKN2KO PKN2 KO matrisome signature predicts poor outcome in pancreatic and other solid human cancers. Our data indicate that suppressing PSC myofibroblast differentiation function can limit important stromal tumour suppressive mechanisms, while promoting a switch to a cancer-supporting CAF phenotype.
2021-11-19 | GSE189027 | GEO