Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE253639 | GEO | 2024/07/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

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 | GSE253368 | GEO

mRNA gene expression of colon fibroblasts isolated from mouse colon

2024-07-02 | GSE253546 | GEO

Contextual cues from cancer cells govern CAF heterogeneity [scRNA-seq]

Project description:Cancer cells function as primary architects of the tumor microenvironment. Yet, the molecular features of cancer cells that govern stromal cell phenotypes remain unclear. Here, we show that cancer-associated fibroblast (CAF) heterogeneity is driven by lung adenocarcinoma (LUAD) cells at either end of the epithelial-to-mesenchymal transition (EMT) spectrum. LUAD cells that have high expression of the EMT-activating transcription factor ZEB1 reprogram CAFs through a ZEB1-dependent secretory program and direct CAFs to the tips of invasive projections through a ZEB1-driven CAF repulsion process. EMT, in turn, sensitizes LUAD cells to pro-metastatic signals from CAFs. Thus, CAFs respond to contextual cues from LUAD cells to promote metastasis.

2021-04-09 | GSE166479 | GEO

Contextual cues from cancer cells govern CAF heterogeneity [Bulk RNA-seq]

2021-04-09 | GSE166478 | GEO

Twist1 knockdown in two gastric cancer-associated fibroblast lines

Project description:Primary human gastric cancer-associated fibroblast (CAF) cultures (CAF14 and CAF32) were establised from 2 gastrectomy specimens. Silencing the expression (loss-of-function effect) of Twist1 in CAFs showed candidate target genes regulated by Twist1 and abrogated their tumor-promoting properties. Experiment design: two gastric CAFs (CAF14 adn CAF32, respectively) were establised from two gastric cancer patients and Twist1 knockdown studies were performed using shRNA.

2014-10-28 | E-GEOD-62738 | biostudies-arrayexpress

Prrx1 is a Master Transcription Factor of myofibroblastic Cancer-Associated Fibroblasts [Human_CAF_ChIP_seq]

Project description:Although cancer associated fibroblasts (CAF) play a critical role in cancer progression, their identities are still unknown. Because cells’ own identity is determined by core regulatory circuit (CRC) comprising master transcription factors (TFs), it is critical to find CAF’s master TF. Therefore, we attempt to find master TF of CAF through the extensive screening of single cell RNA-seq database of cancer tissues, and discovered Prrx1, master regulator of embryonic mesenchymal cells, as candidate for master TF of CAF. Prrx1 was abundantly expressed in CAFs with significant correlation with unfavorable clinical outcomes. Furthermore, Prrx1 in fibroblasts dramatically enhanced tumor progression and metastasis in fibroblast-specific Prrx1 inducible mice. On the other hand, tumor formation was severely inhibited in conditional Prrx1 knock-down mice. Finally, we confirmed that Prrx1 is a master TF of CAF and normal fibroblast executing wound healing program using ChIP-SEQ, CRC modeling, and in vivo validation. Furthermore we also revealed that targeting Prrx1 in fibroblast alone induced complete remission of chemotherapy-resistant cancer in preclinical mouse experiments.

2021-12-31 | GSE169601 | GEO

Prrx1 is a Master Transcription Factor of myofibroblastic Cancer-Associated Fibroblasts [Murine_Wound_Tissue_scRNAseq]

2021-12-31 | GSE169704 | GEO

Prrx1 is a Master Transcription Factor of myofibroblastic Cancer-Associated Fibroblasts [Murine_Fibroblast_RNA_seq]

2021-12-31 | GSE169703 | GEO

Prrx1 is a Master Transcription Factor of myofibroblastic Cancer-Associated Fibroblasts [Murine_co-culture_RNA_seq]

2021-12-31 | GSE169697 | GEO

Prrx1 is a Master Transcription Factor of myofibroblastic Cancer-Associated Fibroblasts [Murine_Fibroblast_ChIP_seq]

2021-12-31 | GSE169723 | GEO