Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from breast cancer tumor-initiating cells

ABSTRACT: We have generated tumorigenic (S2N) and non-tumorigenic (S2), normal-like to basal-like breast cancer cell lines from primary tumors. At high in vivo inoculation cell numbers of 10^6 cells/mouse both S2N and S2 monolayer as well as sphere culture cells grew at similar rates. However, at low inoculation cell numbers down to 10^3 cells only S2N sphere cells generated xenograft tumors. mRNA profiling revealed a unique cluster pattern of the tumorigenic S2N sphere cells, but a detailed analysis of TIC relevant transcription factors like Oct3, Sox and Nanog family members, Myc, Slug or Twist1 revealed no consistently increased expression in the highly tumorigenic cell lines. Our data indicate that the intrinsic genetic and functional markers investigated are not solely indicative of the in vivo tumorigenicity of putative breast tumor-initiating cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE32526 | GEO | 2012/12/21

SECONDARY ACCESSION(S): PRJNA147827

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from breast cancer tumor-initiating cells

Project description:We have generated tumorigenic (S2N) and non-tumorigenic (S2), normal-like to basal-like breast cancer cell lines from primary tumors. At high in vivo inoculation cell numbers of 10^6 cells/mouse both S2N and S2 monolayer as well as sphere culture cells grew at similar rates. However, at low inoculation cell numbers down to 10^3 cells only S2N sphere cells generated xenograft tumors. mRNA profiling revealed a unique cluster pattern of the tumorigenic S2N sphere cells, but a detailed analysis of TIC relevant transcription factors like Oct3, Sox and Nanog family members, Myc, Slug or Twist1 revealed no consistently increased expression in the highly tumorigenic cell lines. Our data indicate that the intrinsic genetic and functional markers investigated are not solely indicative of the in vivo tumorigenicity of putative breast tumor-initiating cells. 4 samples with 3 replicates each

2012-12-21 | E-GEOD-32526 | biostudies-arrayexpress

Amplification of RANK- and c-Met-mediated signaling promotes metastatic colonization

Project description:We found that RANKL, expressed by cancer cells or derived from exogenous sources, consistently induced human prostate, breast, kidney, lung and liver cancer cells to colonize or metastasize to bone in an animal model of cancer bone metastasis. RANK-mediated signaling established a premetastatic niche through a forward feedback loop by inducing RANKL and c-Met expression and downstream signaling via upregulation of master regulator transcription factors regulating EMT (Twist1, Slug, Zeb1, Zeb2), stem cells (Sox2, Myc, Oct3/4 and Nanog), neuroendocrine cells (Sox 9, HIF-1α and FoxA2) and osteomimicry (c-Myc/Max, Sox2, Sox9, HIF1α and Runx2). Abrogating RANK or its downstream signaling network, c-Myc/Max or c-Met, abolished PCa skeletal metastasis in mice. We observed that a small number of RANKL-expressing PCa cells can initiate bone and soft tissue metastases by recruiting non-tumorigenic or bystander PCa or host cells from the circulation or at metastatic sites to co-colonize bone. The recruited bystander PCa cells assume the phenotypes of RANKL-expressing PCa cells by expressing increased c-Met, phosphorylated c-Met and RANKL. RANKL expression at a single cell level in primary PCa tissues predicted disease-specific survival, reflecting the significant role of RANKL-RANK signaling in the development of lethal bone metastasis. Global gene expression analysis perturbed by RANKL in LNRANKL compared to LNNeo cells.

2014-02-06 | E-GEOD-48432 | biostudies-arrayexpress

Twist1 and Slug mediate H2A.X-regulated epithelial-mesenchymal transition in breast cells

Project description:The epithelial-mesenchymal transition (EMT) is thought to be essential for cancer metastasis. While chromatin remodeling is involved in EMT, histone variants contribution in EMT remains poorly investigated. Recently, we showed that silencing or removal of the histone variant H2A.X induced mesenchymal-like characteristics, including activation of the EMT transcription factors, Slug and ZEB1, in human colon cancer cells. Here, we provide the evidence that H2A.X loss in human non-tumorigenic breast cell line MCF10A results in a robust EMT activation, as substantiated by a genome-wide expression analysis. Cells deficient for H2A.X exhibit enhanced migration and invasion, along with an activation of a set of mesenchymal genes and a concomitant repression of epithelial genes. In the breast model, the EMT-related transcription factor Twist1 cooperates with Slug to regulate EMT upon H2A.X loss. Of interest, H2A.X expression level tightly correlates with Twist1, and to a lesser extent with Slug in the panel of human breast cancer cell lines of the NCI-60 datasets. These new findings indicate that H2A.X is involved in the EMT processes in cells of different origins but pairing with transcription factors for EMT may be tissue specific.

2016-06-21 | GSE80180 | GEO

Amplification of RANK- and c-Met-mediated signaling promotes metastatic colonization

2014-02-06 | GSE48432 | GEO

The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer

Project description:Gene expression profile of STAT-signaling tumor-initiating cells (TIC) in breast xenograft models

2024-12-09 | GSE276789 | GEO

Analysis of gene expression change due to knockdown of Slug expression in a basal-subtype breast cancer cell line, MCFDCIS.

Project description:Analysis of gene expression change due to knockdown of Slug expression in a basal-subtype breast cancer cell line, MCFDCIS. Total RNA isolated from MCFDCIS cells transfected with control or Slug specific siRNA.

2016-08-11 | E-GEOD-72011 | biostudies-arrayexpress

Expression data from highly purified MMTV-Neu Tumor Initiating Cells (TICs) and the non-TIC CD24- fraction

Project description:The cancer stem cell model maintains that tumors are organized in a hierarchy driven by tumor initiating cells (TICs), and that patient survival inversely correlates with TIC gene expression. Here we generated a prognostic signature for HER2+ breast cancer from TICs purified from MMTV-Her2/Neu mammary tumors. TICs from this model, identified as Lin-:CD24+:JAG1- at a frequency of 2-5% by serial and single cell transplantation assays, showed elevated expression of proliferation genes and low expression of differentiation genes (compared to non-TIC fraction CD24- of the same tumor). We used microarrays to detect differentially expressed genes in the TIC fraction compared to the non-TIC fraction of the same tumor Cells from each primary tumor were separated by FACS into TIC and non-TIC fractions and total RNA was extracted and hybridized on Affymetrix microarrays.

2011-05-28 | E-GEOD-29590 | biostudies-arrayexpress

Distinct EMT programs control normal stem cells and cancer stem cells of mammary tissue

Project description:Cancer stem cells (CSCs) are proposed to be responsible for metastatic dissemination and clinical relapse in a variety of cancers. Analogies between CSCs and normal tissue stem cells (SC) has led to the notion that CSCs often co-opt the normal SC program of their tissue-of-origin. The cell-biological program termed epithelial-mesenchymal transition (EMT) has been found to encourage entrance of normal and neoplastic mammary cells into the corresponding SC states. Using genetically engineered knock-in reporter mouse lines, we demonstrate that in the murine mammary lineage, the paralogous EMT-inducing transcription factors Snail and Slug, are selectively exploited by CSCs and normal SCs respectively. Slug, when expressed at physiological levels, only activates a partial EMT program and is dispensable in CSCs. In contrast, Snail drives a far more complete transition into the mesenchymal state and controls both tumor-initiation and metastatic dissemination. Consistent with their functional distinctions, Snail controls far more target genes than Slug, and their distinct functions are determined by their divergent N-terminal domains. Our findings underscore fundamental distinctions between the SC program operating in normal and neoplastic SCs, and hint for potential avenues of selective therapeutic elimination of breast CSCs. We sought to understand differential ability to activate the EMT program in breast cancer cells by transcription factors Snail and Slug. Hence, we mapped genome-wide Snail and Slug binding sites in murine MMTV-PyMT breast cancer cell lines that express high level of Snail or high level of Slug respectively. Specifically, we performed Snail ChIP seq in the mesenchymal pBl.3G cells, and Slug ChIP-seq in the epithelial pBl.1G cells.

2015-09-02 | E-GEOD-61198 | biostudies-arrayexpress

Convergence of oncogenic and hormone receptor pathways promotes pro-metastatic phenotypes.

Project description:Cyclin D1b is a splice variant of the cell cycle regulator Cyclin D1 and is known to harbor divergent and highly oncogenic functions in human disease. While Cyclin D1b is induced during disease progression in many cancer types, the mechanisms underlying Cyclin D1b function remain poorly understood. Herein, models of human disease were utilized to resolve the downstream pathways requisite for the pro-tumorigenic functions of Cyclin D1b. Specifically, it was shown that Cyclin D1b modulates the expression of a large transcriptional network that cooperates with AR signaling to enhance tumor cell growth and invasive potential. Notably, Cyclin D1b promoted AR-dependent activation of genes associated with metastatic phenotypes. Further exploration determined that transcriptional induction of SNAI2 (Slug) was essential for Cyclin D1b- mediated proliferative and invasive properties, implicating Slug as a critical driver of disease progression. Importantly, Cyclin D1b expression highly correlated with that of Slug in clinical samples of advanced disease. Further, in vivo analyses provided strong evidence that Slug enhances both tumor growth and homing to distal soft tissues. Collectively, these findings reveal the underpinning mechanisms behind the pro-tumorigenic functions of Cyclin D1b, and demonstrate that the convergence of the Cyclin D1b-AR and Slug pathways results in the activation of processes critical for the promotion of lethal tumor phenotypes. Analysis of transcriptomes under the control of individual D-type cyclin isoforms in the hormone dependent prostate cancer cell line LNCaP in the presence and absence of androgen. LNCaP cells cultured in charcoal dextran treated media were transduced with virus encoding Cyclin D1a, Cyclin D1b, or control GFP for 24 hours in biological triplicate. Cells were then stimulated with either 1nM DHT or 0.01% EtOH (vehicle control) for 16 hours and harvested for RNA

2013-03-31 | E-GEOD-40794 | biostudies-arrayexpress

Tumorspheres from transformed fibroblasts highlight the great plasticity of differentiated tumorigenic cells

Project description:Tumors are heterogeneous tissues. A subpopulation of cells with stemness features (cancer stem cells: CSCs) has been implicated in tumor maintenance and progression. There is evidence that CSCs can originate from tumor cell dedifferentiation. Here we used in vitro transformed human fibroblasts (cen3tel cells) and the tumorsphere assay to search for and possibly characterize CSCs from differentiated transformed cells. To obtain tumorspheres, cen3tel cells were grown in the absence of serum and in the presence of growth factors. Sphere cells were analysed for the expression of specific genes and their genome wide gene expression profiles relative to cells grown in adhesion were determined by microarray analysis. Cen3tel cells formed spheres showing self-renewal capacity and Sox2 overexpression, suggesting that they contained a subset of cells with CSC-like features. Sphere cells displayed the deregulation of a c-MYC-miR-34a circuitry, likely associated with cell protection from apoptosis. Gene expression profiles of sphere cells revealed an extensive transcriptional reprogramming. Genes upregulated in tumorspheres identified processes related to tumorigenesis and stemness, such as chromatin organization, cholesterol biosynthetic pathway, apoptosis suppression, immunity and defense, interferon mediated immunity and cytokine and chemokine mediated signalling pathway. However, sphere cells were only slightly more tumorigenic in vivo than adherent cells. Our results indicate that tumorigenic cells obtained from differentiated human fibroblasts are highly plastic and can acquire cancer stem cells properties. However, tumorsphere cells are not the main tumorigenic population, highlighting a further level of complexity in tumor heterogeneity.

2018-12-25 | GSE109787 | 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