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An epigenetically distinct breast cancer cell subpopulation promotes collective invasion

ABSTRACT: A distinct highly invasive subpopulation was identified in breast cancer cell lines. The molecular characteristics of these cells was investigated, revealing a set of genes whose high expression confers the ability to invade.

ORGANISM(S): Homo sapiens

PROVIDER: GSE58643 | GEO | 2014/06/19

SECONDARY ACCESSION(S): PRJNA253065

REPOSITORIES: GEO

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An epigenetically distinct breast cancer cell subpopulation promotes collective invasion

Project description:A distinct highly invasive subpopulation was identified in breast cancer cell lines. The molecular characteristics of these cells was investigated, revealing a set of genes whose high expression confers the ability to invade. Total RNA isolated from the invasive subpopulation from 2 cells lines was compared to total RNA isolated from 2 noninvasive populations.

2014-06-19 | E-GEOD-58643 | biostudies-arrayexpress

An epigenetically distinct breast cancer cell subpopulation promotes collective invasion

Project description: Not available

| S-ECPF-GEOD-58643 | biostudies-other

An epigenetically distinct breast cancer cell subpopulation promotes collective invasion.

Project description: Not available

| S-EPMC4463195 | biostudies-literature

Cell plasticity identifies an epigenetically distinct cancer subpopulation

Project description:Cell plasticity identifies an epigenetically distinct cancer subpopulation driving drug resistance and progression

| PRJEB12150 | ENA

TGFβ1 promotes collective invasion of oncogenically transformed intestinal organoids by inducing partial epithelial-mesenchymal transition independently of Snail1 and Zeb1

Project description:Cancer cells simultaneously featuring epithelial and mesenchymal traits appear particularly competent to invade and metastasize. However, genetic prerequisites and signaling pathways promoting such partial epithelial-to-mesenchymal transitions (EMT) remain obscure. Here we report that murine intestinal organoids with hyperactive Wnt and MAPK signaling, and mutant Trp53 are purely epithelial and non-invasive in vitro, but initiate a collective invasion program when treated with TGFβ1. Invasive organoids reciprocally interact with the extracellular matrix (ECM), and autonomously deposit and remodel components thereof. Although cells at the organoid/ECM interface shed certain epithelial characteristics, invasive organoids largely maintain epithelial gene expression while concomitantly upregulating a mesenchymal program. TGFβ1-induced phenotypic changes involve canonical, Smad4-dependent signaling, yet, are unimpeded by knockout of Snai1 and Zeb1 - otherwise key regulators of epithelial-to-mesenchymal transitions. The finding of TGFβ1-inducible, Snail1/Zeb1-independent collective invasion of oncogenically transformed intestinal organoids provides novel mechanistic insights and broadens the spectrum of context-dependent manifestations of partial EMT.

2022-01-24 | GSE156553 | GEO

Triple negative breast tumors contain heterogeneous cancer cells expressing distinct KRAS-dependent collective and disseminative invasion programs

Project description:Inter-patient and intra-tumoral heterogeneity complicate the identification of predictive biomarkers and effective treatments for basal triple negative breast cancer (b-TNBC). Invasion is the initiating event in metastasis and can occur by both collective and single-cell mechanisms. We cultured primary organoids from a b-TNBC genetically engineered mouse model in 3D collagen gels to characterize their invasive behavior. We observed that organoids from the same tumor presented different phenotypes that we classified as non-invasive, collective and disseminative. To identify molecular regulators driving these invasive phenotypes, we developed a workflow to isolate individual organoids from the collagen gels based on invasive morphology and perform RNA sequencing. We next tested the requirement of differentially regulated genes for invasion using shRNA knock-down. Strikingly, KRAS was required for both collective and disseminative phenotypes. We then performed a drug screen targeting signaling nodes upstream and downstream of KRAS. We found that inhibition of EGFR, MAPK/ERK, or PI3K/AKT signaling reduced invasion. Of these, ERK inhibition was striking for its ability to potently inhibit collective invasion and dissemination. We conclude that different cancer cells in the same b-TNBC tumor can express different metastatic molecular programs and identified KRAS and ERK as essential regulators of collective and single cell dissemination.

2023-01-03 | GSE215069 | GEO

DCLK1 Marks a Morphologically Distinct Subpopulation of Cells with Stem Cell Properties in Pre-invasive Pancreatic Cancer

Project description:As in other tumor types, progression of pancreatic cancer may require a functionally unique population of cancer stem cells. Although such cells have been identified in many invasive cancers, is not clear whether they emerge during early or late stages of tumorigenesis. Using mouse models and human pancreatic cancer cell lines, we investigated whether pre-invasive pancreatic neoplasia contains a subpopulation of cells with distinct morphologies and cancer stem cell like properties. Whole transcriptome anlaysis of AcTub Hi vs AcTub Low cells. Cells were labeled with an acetylated alpha tubulin antibody that recognized epitopes on the cell surface (AAT+). AcTub Hi vs Low cells were FACS sorted from the human pancreatic cancer cell lines CFPAC and AsPC1 CFPAC and AsPC1 cells were labeling with AcTub (acetylated alpha tubulin antibody) and then FACS sorted based on high or low levels of AcTub, and microarray analyses were run on biological replicates.

2013-11-16 | E-GEOD-52406 | biostudies-arrayexpress

Epigenetically heterogeneous tumor cells direct collective invasion through filopodia-driven fibronectin micropatterning.

Project description: Not available

| S-EPMC7439406 | biostudies-literature

Identification of bistable populations of Porphyromonas gingivalis that differ in epithelial cell invasion.

Project description:Bistable populations of bacteria give rise to two or more subtypes that exhibit different phenotypes. We have explored whether the periodontal pathogen, Porphyromonas gingivalis, exhibits bistable invasive phenotypes. Using a modified cell invasion assay, we show for the first time that there are two distinct sub-types within a population of P.ginigivalis strains NCTC 11834 and W50 that display differences in their ability to invade oral epithelial cells. The highly-invasive sub-types invade cells at 10-30 fold higher levels than the poorly-invasive subtype and remain highly invasive for approximately 12-16 generations. Analysis of the gingipain activity of these sub-types revealed that the highly invasive type had reduced cell-associated arginine specific protease activity. The role of arg-gingipain activity in invasion was verified by enhancement of invasion by rgpAB mutations and by inclusion of an arg-gingipain inhibitor in invasion assays using wild-type bacteria. In addition a population of DeltargpAB bacteria did not contain a hyperinvasive sub-type. Screening of the protease activity of wild-type populations of both strains identified high and low protease sub-types which also showed the corresponding reduction or enhancement of invasive capabilities. Microarray analysis of these bistable populations revealed a putative signature set of genes that include oxidative stress resistance and iron transport genes that might be key to invasion of or survival within epithelial cells. Porphyromonas gingivalis comparison of Invasive V Non-invasive sub-types of NCTC11834 and W50 (samples 1-12 AND High V low protease subtypes (samples 13-24) Samples 1-3 were compared top 4-6 and 7-9 V 10-12 for invasive experiments and similarly for protease strain experiments

2010-08-31 | E-GEOD-23021 | biostudies-arrayexpress

DCLK1 Marks a Morphologically Distinct Subpopulation of Cells with Stem Cell Properties in Pre-invasive Pancreatic Cancer

2013-11-16 | GSE52406 | GEO

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