Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A compositional change in exomiRs during normal fibroblast to cancer-associated fibroblast transition.

ABSTRACT: To understand the role of stromal exomiRs on tumor progression, the count values of exomiRs was compared between the normal and cancer-associated fibroblasts derived from an invasive ductal carcinoma patient.

ORGANISM(S): Homo sapiens

PROVIDER: GSE134022 | GEO | 2019/12/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

A compositional change in exomiRs during normal fibroblast to cancer-associated fibroblast transition.

Project description:A compositional change in exomiRs during normal fibroblast to cancer-associated fibroblast transition.

| PRJNA553539 | ENA

Pericyte-fibroblast transition promotes tumor growth and metastasis

Project description:Vascular pericytes, an important cellular component, in the tumor microenvironment, are often associated with tumor vasculatures and their functions in cancer invasion and metastasis are poorly understood. Here we show that PDGF-BB induces pericyte fibroblast transition (designated as PFT), which significantly contributes to tumor invasion and metastasis. Gain- and loss-of-function experiments demonstrate that the PDGF-BB-PDGFRÎ² signaling promotes PFT in vitro and in in vivo tumors. Genome-wide expression analysis indicates that PDGF-BB-activated pericytes acquire mesenchymal progenitor features. Pharmacological inhibition and genetic deletion of PDGFRÎ² ablate the PDGF-BB-induced PFT. Genetic tracing of pericytes with two independent mouse strains, i.e., TN-AP-CreERT2:R26R-tdTomato and NG2:R26R-tdTomato, shows that PFT cells gains stromal fibroblast and myofibroblast markers in tumors. Importantly, co-implantation of PFT cells with less-invasive tumor cells in mice markedly promotes tumor dissemination and invasion, leading to an increased number of circulating tumor cells (CTCs) and metastasis. Our findings reveal a novel mechanism of vascular pericytes in PDGF-BB-promoted cancer invasion and metastasis by inducing PFT and thus targeting PFT may offer a new treatment option of cancer metastasis. Pericytes were isolated and treated with PDGF-BB or control for 1 or 5 days

2016-08-24 | E-GEOD-85955 | biostudies-arrayexpress

Pericyte-fibroblast transition promotes tumor growth and metastasis

Project description:Vascular pericytes, an important cellular component, in the tumor microenvironment, are often associated with tumor vasculatures and their functions in cancer invasion and metastasis are poorly understood. Here we show that PDGF-BB induces pericyte fibroblast transition (designated as PFT), which significantly contributes to tumor invasion and metastasis. Gain- and loss-of-function experiments demonstrate that the PDGF-BB-PDGFRβ signaling promotes PFT in vitro and in in vivo tumors. Genome-wide expression analysis indicates that PDGF-BB-activated pericytes acquire mesenchymal progenitor features. Pharmacological inhibition and genetic deletion of PDGFRβ ablate the PDGF-BB-induced PFT. Genetic tracing of pericytes with two independent mouse strains, i.e., TN-AP-CreERT2:R26R-tdTomato and NG2:R26R-tdTomato, shows that PFT cells gains stromal fibroblast and myofibroblast markers in tumors. Importantly, co-implantation of PFT cells with less-invasive tumor cells in mice markedly promotes tumor dissemination and invasion, leading to an increased number of circulating tumor cells (CTCs) and metastasis. Our findings reveal a novel mechanism of vascular pericytes in PDGF-BB-promoted cancer invasion and metastasis by inducing PFT and thus targeting PFT may offer a new treatment option of cancer metastasis.

2016-08-24 | GSE85955 | GEO

Genomic alterations during the in situ to invasive ductal breast carcinoma transition shaped by the immune system

Project description:Genomic alterations during the in situ to invasive ductal breast carcinoma transition shaped by the immune system

2020-12-01 | GSE144020 | GEO

Transcription profiling of human ductal carcinoma in situ (DCIS) and invasive component (IDC) from 9 breast cancers to identify novel molecular markers characterizing the transition from DCIS to IDC.

Project description:This is a matched-pair analysis of ductal carcinoma in situ (DCIS) and invasive component (IDC) of nine breast ductal carcinoma to identify novel molecular markers characterizing the transition from DCIS to IDC for a better understanding of its molecular biology.

2007-10-02 | E-GEOD-3893 | biostudies-arrayexpress

Cancer-associated fibroblast driven paracrine IL-6/STAT3 signalling promotes migration and dissemination in invasive lobular carcinoma

Project description:Invasive Lobular Carcinoma (ILC) is an under-studied yet common subtype of breast cancer. A key feature of ILC tumours, due to their single-file invasive growth pattern, is a high stromal content and in particular, an abundance of cancer-associated fibroblasts (CAFs). We identified that IL-6 secreted from primary ILC patient-derived CAFs drives STAT3 activation in ILC cell lines and found that IL6, STAT3, pSTAT3 and subsequent downstream gene expression induced by IL-6 within CAF conditioned media is upregulated in ILC tumours compared to Invasive Ductal Carcinoma tumours, the most common subtype of breast cancer. This dataset contains 3`-mRNAseq data from ILC cell lines (SUM44PE and MDA-MB-134VI) and patient-derived organoids (HCI-013 and HCI-018) stimulated with either recombinant human IL-6 (10 ng/ml) for 24 hours or 1 week or SUM44PE cells stimulated with CAF conditioned media (CAF CM)collected from ED26 primary ILC CAFs (characterised here: doi.org/10.3390/cancers14040904) +/- an IL-6 neutralising antibody. RNA was extracted using Qiagen RNeasy mini-kit and libraries were prepared using QuantSeq 3’ mRNA-Seq Library Prep Kit (FWD) for Illumina (Lexogen Inc, #015).

2024-10-11 | GSE276108 | GEO

Proteome and secretome of human mammary normal fibroblasts and CAF

Project description:The secretome of cancer and stromal cells generates a microenvironment which contributes to tumour cell invasion and angiogenesis. Here, we compare the secretome of human mammary normal fibroblasts and cancer-associated fibroblasts (CAF). We discover that the chloride intracellular channel protein 3 (CLIC3) is an abundant component of the CAF secretome. Secreted CLIC3 promotes invasive behaviour of endothelial cells to drive angiogenesis and increases invasiveness of cancer cells both in vivo and in 3D cell culture models, and this requires active transglutaminse-2 (TGM2). CLIC3 acts as a glutathione-dependent oxidoreductase which reduces TGM2 and regulate TGM2 binding to its cofactors. Finally, CLIC3 is secreted also by cancer cells, is abundant in the stromal and tumour compartments of aggressive ovarian cancers, and its levels correlate with poor clinical outcome. This work reveals an unprecedented invasive mechanism whereby the secretion of a glutathione-dependent oxidoreductase drives angiogenesis and cancer progression by promoting TGM2-dependent invasion.

2016-12-13 | PXD002444 | Pride

IGFBP2 secretion by mammary adipocytes limits breast cancer invasion

Project description:The progression of noninvasive ductal carcinoma in situ to invasive ductal carcinoma for patients with breast cancer results in a significantly poorer prognosis and is the precursor to metastatic disease. In this work, we have identified insulin-like growth factor–binding protein 2 (IGFBP2) as a potent adipocrine factor secreted by healthy breast adipocytes that acts as a barrier against invasive progression. In line with this role, adipocytes differentiated from patient-derived stromal cells were found to secrete IGFBP2, which significantly inhibited breast cancer invasion. This occurred through binding and sequestration of cancer-derived IGF-II. Moreover, depletion of IGF-II in invading cancer cells using small interfering RNAs or an IGF-II–neutralizing antibody ablated breast cancer invasion, highlighting the importance of IGF-II autocrine signaling for breast cancer invasive progression. Given the abundance of adipocytes in the healthy breast, this work exposes the important role they play in suppressing cancer progression and may help expound upon the link between increased mammary density and poorer prognosis.

2023-07-13 | PXD036479 | Pride

Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer

Project description:This SuperSeries is composed of the following subset Series: GSE41194: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 1) GSE41196: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 2) GSE41197: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 3) GSE41198: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 4 stroma) GSE41227: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 4 Epithelial) Refer to individual Series

2012-09-29 | E-GEOD-41228 | biostudies-arrayexpress

A genomic ruler to assess oncogenic transition between breast tumor and stroma

Project description:Genome-wide gene expression changes were determined in histopathologically normal breast tissue in 33 women undergoing mastectomy for stage II and III primary invasive ductal carcinoma at serial distances in three dimensions from the tumor. Gene expression was determined by genome-wide mRNA analysis and subjected to metagene mRNA characterization

2018-09-19 | GSE120129 | 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