Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

2d88259c-2f3f-4871-ae35-0dec8c5c8bc1 - samples

ABSTRACT: 180502: RNA-Sequencing data of cocultured matched CRC patient (P4) derived normal fibroblasts (NFs), cancer associated fibroblasts (CAFs) and tumor spheroids. 200503_coculture: RNA-Sequencing data of cocultured CRC patient derived normal fibroblasts (NFs) or cancer associated fibroblasts (CAFs) (P16, P19, P22, P32, P41, P42) and tumor spheroids (HT29). 200503_il1b: RNA-Sequencing data of IL-1ÃŽÂ² stimulated fibroblasts (NFs and CAFs) Cole: scRNA-sequencing of matched CRC tumour samples and normal tissue counterparts derived from 3 patients. 220501: RNA-Sequencing of FACS sorted IL1R1 high and IL1R1 low CT5.3 CAFs

PROVIDER: EGAD00001010322 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

Enhanced antigen cross-presentation in human colorectal cancer-associated fibroblasts through upregulation of the lysosomal protease Cathepsin S

Project description:Cross-presentation of exogenous antigens in HLA-class I molecules by professional antigen presenting cells (APCs) is crucial for CD8+ T cell function. Recent murine studies show that several non-professional APCs, including cancer-associated fibroblasts (CAFs) also possess this capacity. It is currently unknown whether human CAFs are able to cross-present exogenous antigen, which molecular pathways are involved in this process and how this ultimately affects tumor-specific CD8+ T cell function. Here we show that human colorectal cancer (CRC)-derived CAFs display an enhanced capacity to cross-present neoantigen-derived synthetic long peptides (SLPs) when compared to normal colonic fibroblasts. Importantly, cross-presentation of antigens required the lysosomal protease Cathepsin S. Cathepsin S expression by CAFs was detected in situ in human CRC tissue, was upregulated in ex vivo cultured CRC-derived CAFs and showed increased expression in normal fibroblasts after exposure to CRC-conditioned medium. Cognate interaction between CD8+ T cells and cross-presenting CAFs suppressed T cell function, reflected by decreased cytotoxicity, reduced activation (CD25, CD137) and increased exhaustion (TIM3) marker expression. Our data indicate that CAFs may directly suppress tumor-specific T cell function in an antigen-dependent fashion in human CRC.

2022-03-03 | PXD029507 | Pride

RNA-Sequencing data of patient derived normal fibroblasts (NFs), cancer associated fibroblasts (CAFs) and tumor spheroid samples

Project description:RNA-Sequencing data of patient derived normal fibroblasts (NFs), cancer associated fibroblasts (CAFs) and tumor spheroid samples performed in the context of the characterization of an IL1R1 positive CAF population in CRC tumour samples.

| EGAS00001007205 | EGA

Co-cultivation of colorectal cancer cells and human skin fibroblasts in 3D collagen gel and comparison of co-cultivated fibroblasts with CAFs

Project description:Despite the growing recognition of the role of the stroma in cancer growth, invasive behavior and metastasis, the exact mechanisms of its participation remain unclear. We have explored the relationships between the epithelial/mesenchymal (E/M) state of colorectal cancer cells, their ability to activate fibroblasts, and the expression of collagen related genes. To this end, we studied (i) co-cultures of colorectal cancer cells with different hybrid E/M states and normal fibroblasts in a collagen matrix and (ii) patient-derived cancer-associated fibroblasts (CAFs). Using RNA-sequencing, we found that the different cancer cells can activate normal fibroblasts, which could form dense collagen networks. The functional enrichment analysis of differentially expressed genes indicates more mesenchymal phenotype and greater motility of SW480 cells compared to HT29 cells. The genes related to collagen biosynthesis and catabolism tend to be more active in SW480 cells rather than HT29 cells. Moreover, LOXL2 and LOXL3 genes, which are necessary for collagen fibril organization, are SW480 specific, which may indicate greater input of this cell line in collagen remodeling compared to HT29 cells. The expression of several CAF marker genes is activated in NFs upon co-cultivation with HT29 and SW480. Interestingly, a more-epithelial cell line HT29 activates the fibroblasts to a greater extent, than does SW480. The co-cultivation of colon cancer cell lines HT29 or SW480 with NFs leads to the activation of collagen biosynthesis and collagen fibril organization genes in NFs. Our findings suggest that the normal fibroblasts, activated by cancer cells, contribute to the organization of the extracellular matrix. Therefore, targeting the ability of cancer cells to activate normal fibroblasts can be considered as a new therapeutic strategy.

2020-10-30 | GSE155343 | GEO

Mimicking tumor cell heterogeneity of colorectal cancer in a patient-derived organoid-fibroblast model

Project description:Patient derived organoids (PDOs) have been established as a 3D culture model which closely recapitulates the in vivo tumor biology. However, one limitation of this culture model is the lack of tumor microenvironment which has a significant role in tumor progression and drug response. To address this, we established and molecularly characterized a novel 3D co-culture model of colorectal cancer (CRC) based on PDOs and patient matched fibroblasts. Both normal and cancer associated fibroblasts, NFs and CAFs respectively, were able to support organoid growth without addition of niche factors to the media. Additionally, co-cultures showed closer resemblance to primary patient material than organoid mono-cultures as evaluated by histology. Finally, RNA gene expression signatures of tumor cells and fibroblasts isolated from mono- or co-cultures demonstrated that co-cultures support greater cell type heterogeneity. In this proteomics dataset we compared pairs of NFs and CAFs derived from five patients. Collectively, we present a newly established human derived organoid-fibroblast model which, closely recapitulates in vivo tumor heterogeneity and involves the tumor microenvironment.

2023-03-14 | PXD032047 | Pride

Fibroblasts: Normal fibroblasts vs. Carcinoma-associated fibroblasts

Project description:Transcriptional profiling of human carcinoma-associated fibroblasts (CAFs) comparing control normal fibroblasts (NFs). NFs derived from normal tissues and CAFs derived from the patients with oral cancer were identified by immunocytochemistry. Goal was to determine differentially expressed lncRNAs between NFs and CAFs.

2024-01-08 | GSE164473 | GEO

The origin and contribution of the tumor stroma in colorectal carcinogenesis

Project description:Background and aims Cancer-associated fibroblasts (CAFs) play a critical role in colorectal cancer (CRC) progression. However, the precise cellular origins of the tumor stroma remain unknown, making it challenging to therapeutically target the tumor mesenchyme. Here, we aimed to identify key cellular contributors to and components of the CRC mesenchyme associated with poor prognosis. Methods We used a mouse model of inflammation-associated CRC in 5 different genetic fate-mapping transgenic mouse lines to characterize the origins of the CRC stroma. To identify a potential therapeutic target expressed by the CRC stroma, RNA-sequencing of fluorescence-activated cell sorting (FACS)-purified CRC stromal cells was performed. CRC patient RNA-sequencing data (n=621) and tissue microarray (n=101) were used to examine the prognostic significance of marker expression. Results We found that approximately half of the CRC CAFs marked by α-smooth muscle actin (αSMA) in a mouse model of CRC emerge through proliferation. Lineage tracing experiments revealed that intestinal leptin receptor (Lepr)-lineage stromal cells expanded and contributed to 75% of the αSMA+ proliferating CAFs. Notably, no αSMA+ CAFs arose from Krt19-lineage epithelial cells or bone marrow-derived cells. Moreover, RNA-sequencing of FACS-purified CRC mesenchymal cells identified MCAM as a CRC stroma-specific marker, which is expressed by Lepr-lineage cells. Analysis of human CRC samples showed that high MCAM expression driven, in part, by TGF-β was independently prognostic of poor overall survival. Conclusion Our data identify intestinal Lepr-lineage cells as a major source of the tumor stroma in CRC and suggest that targeting MCAM+ cells may serve as an attractive therapeutic approach to restrain CRC progression.

2022-11-01 | GSE162508 | GEO

Gene expression profiles of SKOV3 tumor cells that could form heterotypic spheroids with high grade serous ovarian cancer derived cancer-associated fibroblasts, and those remaining individual SKOV3 cells in non-adherent (NAD) coculture condition.

Project description:Interaction between stromal cells and the tumor greatly influences tumor initiation and progression. Cancer-associated fibroblasts (CAFs) are the major component of tumor stroma and play a key role in ovarian cancer (OC) cells adhesion and metastasis. CAFs were found abundantly in primary tumor and metastases, as well as in malignant ascites of high grade serous OC patients, underscoring that CAFs modulate OC cells phenotype and facilitate disease exacerbation along OC progression. Studies of CAFs exertion on OC mainly focused on the influence of CAFs conditioned medium (CM) influence of tumor cells phenotype, while ignoring the fact that CAFs are supposed to be in intimate contact with neoplastic cells in tumor mass, and that CAFs also form compact heterotypic spheroids with ascitic tumor cells in malignant ascites. We hypothesized that uncovering the underlying molecules that mediate tumor cells binding with CAFs could aid in developing measures destroying the pro-carcinogenic heterotypic spheroids in malignant ascites. In this study, gene expression profiling was completed for individual SKOV3, and magnetic sorted SKOV3 cells that form heterotypic spheroids with 4 cases of high grade serous OC derived CAFs. By comparing the expression data of SKOV3 cells in individual group with that in spheroid group, we identified a set of differential expressed genes. This study revealed the heterogeneity of ascitic tumor cells and raised potent therapeutical targets in destroying of the heterotypic spheroids in malignant ascites of OC. We used microarrays to profile the mRNA expression of SKOV3 tumor cells that could or not form heterotypic spheroids with CAFs, in order to identify molecules that potentially mediate the combination between tumor cells and CAFs.

2018-09-13 | GSE98154 | GEO

Proteome Profiling Identifies Markers for Inflammation-Related Tumor-Fibroblast Interaction in Colorectal Cancer

Project description:Inflammation has been identified as an important factor in cancer development and progression, including colorectal cancer [CRC]. To determine the role of inflammation and the specific contribution of activated fibroblasts in cancer development and progression we analyzed six human CRC tissue specimens and paired normal adjacent mucosa samples by LS/MS-MS. Amongst other, indeed several inflammation associated proteins were found differentially expressed compared to normal colonic mucosa. Two candidate molecules, SPARC and THBS2 were recently identified as proteins of a fibroblast inflammation signature. Analysis of public available RNA expression datasets revealed, that the mRNA of both SPARC and THBS2 are upregulated in CRC, typically in association with the CRC consensus molecular subtype 4 [CMS4]. Immunohistochemistry staining also demonstrated upregulation of SPARC and THBS2 in the tumor stroma compared to normal adjacent mucosa and indicated co-localization with the mesenchymal marker [alpha]SMA. In vitro 3D co-culture experiments with human colon derived fibroblasts and CRC cell lines resulted in enhanced SPARC and THBS2 protein levels when both cell types were cultivated in direct physical contact, compared to fibroblasts or cancer cells alone. This study demonstrates the feasibility of detecting tumor-specific signatures by LC-MS/MS and compatibility with RNA expression datasets. We identified an inflammation signature in CRC tissue and the data emphasized the contribution of activated fibroblasts in these events.

2018-10-17 | PXD006776 | Pride

Hypoxic microenvironment activates GLI2 through synergistic action of TGF-β2 and HIF-1α to confer chemoresistance and poor clinical outcome in colorectal cancer [IlluminaExpr_1_CAF_NF]

Project description:Analysis of gene expression profiles of three cancer-associated fibroblasts (CAFs) and four normal fibroblasts (NFs), which are derived from tumor tissues and adjacent normal mucosa of colorectal cancer patients, respectively.

2019-01-30 | GSE93253 | GEO

Single-Cell Analysis of Human Pancreatic Ductal Adenocarcinoma

Project description:<p>Cancer-associated fibroblasts (CAFs) are major players in the progression and drug resistance of pancreatic ductal adenocarcinoma (PDAC). CAFs constitute a diverse cell population consisting of several recently described subtypes, although the extent of CAF heterogeneity has remained undefined. Here we employ single-cell RNA-sequencing to thoroughly characterize the neoplastic and tumor microenvironment content of human PDAC tumors. Six human PDAC tumor specimens from six patients were collected, and processed for single-cell RNA-sequencing analysis. Adjacent-normal pancreas tissue was also collected from two of the patients. Tumor samples were digested, and fluorescence-activated cell sorting was used to isolate viable cells. For one tumor sample, viable, CD45-negative, CD31-negative, and EpCAM-negative cells were also isolated to enrich for CAFs. The 10X Chromium platform was then used to isolate single cells for RNA-sequencing analysis. This work has demonstrated the differences in immune cell populations between adjacent-normal and tumor tissues, and identified subpopulations of epithelial cells and CAFs present in PDAC tumors. This high-throughput analysis is a resource to better understand the cell populations present in PDAC, and may ultimately aid in the development of more effective therapies for this deadly malignancy.</p>

| phs001840 | dbGaP

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