Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Impact of inhibiting cancer-associated fibroblasts (CAFs)

ABSTRACT: Inhibiting distinct CAF population impairs tumour growth and metastasis

PROVIDER: PRJEB36901 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR4918834_1.fastq.gz	Fastqsanger.gz
	ERR4918834_2.fastq.gz	Fastqsanger.gz
	ERR4918835_1.fastq.gz	Fastqsanger.gz
	ERR4918835_2.fastq.gz	Fastqsanger.gz
	ERR4918836_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Impact of inhibiting cancer-associated fibroblasts (CAFs)

Project description:Inhibiting distinct CAF population impairs tumour growth and metastasis

| PRJEB43908 | ENA

Proteomics reveals NNMT as a master metabolic regulator of cancer associated fibroblasts

Project description:High-grade serous carcinoma has a poor prognosis, owing primarily to its early dissemination throughout the abdominal cavity. Genomic and proteomic approaches have provided snapshots of the proteogenomics of ovarian cancer, but a systematic examination of both the tumour and stromal compartments is critical in understanding ovarian cancer metastasis. We developed a label- free proteomic workflow to analyse as few as 5,000 formalin-fixed, paraffin-embedded cells microdissected from each compartment. The tumour proteome was stable during progression from in situ lesions to metastatic disease; however, the metastasis-associated stroma was characterized by a highly conserved proteomic signature, prominently including the methyltransferase nicotinamide N-methyltransferase (NNMT) and several of the proteins that it regulates. Stromal NNMT expression was necessary and sufficient for functional aspects of the cancer-associated fibroblast (CAF) phenotype, including the expression of CAF markers and the secretion of cytokines and oncogenic extracellular matrix. Stromal NNMT expression supported ovarian cancer migration, proliferation and in vivo growth and metastasis. Expression of NNMT in CAFs led to depletion of S-adenosyl methionine and reduction in histone methylation associated with widespread gene- expression changes in the tumour stroma. This work supports the use of ultra-low-input proteomics to identify candidate drivers of disease phenotypes. NNMT is a central, metabolic regulator of CAF differentiation and cancer progression in the stroma that may be therapeutically targeted.

2019-04-18 | PXD006396 | Pride

Proteomic analysis Carcinoma associated fibroblasts (CAFs) following genetic manipulation of NID2 expression

Project description:Proteomic anlaysis was performed on CAF GFP-1 KRAB, CAF B500 NID2 KRAB and CAF C500 NID2 KRAB cell lines

2024-08-10 | PXD050045 | Pride

Transcriptomic analysis of CAFs with silencing of ANKRD1.

Project description:Stromal cell senescence plays a crucial role in activating cancer-associated fibroblasts (CAFs). The Androgen receptor (AR) function oversees cellular senescence and CAF activation. Here, we identify the mesenchymal-specific transcriptional coregulator ANKRD1 as a key driver of CAF conversion. ANKRD1 is strongly upregulated in CAFs and under direct negative control of AR, and its loss impairs the pro-tumorigenic potential of CAFs. ANKRD1 controls a CAF-specific gene expression program and is associated with poorer survival of HNSCC, lung, and cervical SCC patients. Mechanistically, ANKRD1 binds to the chromatin on CAF gene regulatory regions in a complex with the AP1 transcription factor family. We show that ANKRD1 enhances the AP1 DNA binding activity to CAF gene promoters. Targeting ANKRD1 with the FANA antisense oligonucleotides reverts CAFs into a normal fibroblast, disrupts AP1 complex formation, and blocks CAF’s pro-tumorigenic potential in an orthotopic model of SCC, thus representing an exciting target for stroma-oriented cancer therapy.

2023-11-10 | GSE218214 | GEO

mRNA gene expression of colon fibroblasts isolated from mouse colon

Project description:The EMT-transcription factor ZEB1 is heterogeneously expressed in tumor cells and in cancer-associated fibroblasts (CAFs) in colorectal cancer (CRC). While ZEB1 in tumor cells regulates metastasis and therapy resistance, its role in CAFs is largely unknown. Combining fibroblast-specific Zeb1 deletion with immunocompetent mouse models of CRC, we observe that inflammation-driven tumorigenesis is accelerated, whereas invasion and metastasis in sporadic cancers is reduced upon fibroblast-specific loss of Zeb1. Single-cell transcriptomics, histological characterization and in vitro modelling reveal a crucial role in CAF polarization, promoting myofibroblastic features by restricting inflammatory activation. Zeb1 deficiency impairs collagen deposition and CAF barrier function but increasesd NFκB-mediated cytokine production, jointly promoting lymphocyte recruitment and immune checkpoint activation.

2024-07-02 | GSE253546 | GEO

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

Secretome of cancer-associated fibroblasts (CAFs) influences drug sensitivity in cancer cells

Project description:Resistance is a major problem with effective cancer treatment and the stroma forms a significant portion of the tumor mass but traditional drug screens involve cancer cells alone. Cancer-associated fibroblasts (CAFs) are a major tumor stroma component and its secreted proteins may influence the function of cancer cells. The majority of secretome studies compare different cancer or CAF cell lines exclusively. Here, we present the direct characterization of the secreted protein profiles between CAFs and KRAS mutant-cancer cell lines from colorectal, lung, and pancreatic tissues using multiplexed mass spectrometry. 2573 secreted proteins were annotated, and differential analysis highlighted understudied CAF-enriched secreted proteins, including Wnt family member 5B (WNT5B), in addition to established CAF markers, such as collagens. The functional role of CAF secreted proteins was explored by assessing its effect on the response to 97 anticancer drugs since stromal cells may cause a differing cancer drug response, which may be missed on routine drug screening using cancer cells alone. CAF secreted proteins caused specific effects on each of the cancer cell lines, which highlights the complexity and challenges in cancer treatment and so the importance to consider stromal elements.

2024-05-29 | PXD048307 | Pride

Gene expression of Cancer-associated fibroblasts from orthotopically engrafted murine colon tumors on the single cell level (Sort-Seq)

2024-07-02 | GSE253639 | GEO

Gene expression of Cancer-associated fibroblasts from AOM/DSS autchthonous murine tumors on the single cell level (Sort-Seq)

2024-07-02 | GSE253368 | GEO

Transcriptome analysis of primary normal fibroblasts and matched cancer associated fibroblasts

Project description:To get an insight into the mechanisms for CAF-supported metastasis in breast cancers, we performed RNA-sequencing (RNA-seq) analysis with seven pairs of primary NFs and CAFs.Gene set variation analysis (GSVA) showed significant upregulated expression of genes enriched with cancer metastasis-associated signaling pathways. Besides, we identified CAF signature genes, which have similar patterns in several of these primary CAFs.

2022-12-09 | GSE196354 | 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