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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. 4 samples with 3 replicates each

ORGANISM(S): Homo sapiens

SUBMITTER: Helmut Burtscher

PROVIDER: E-GEOD-32526 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Established breast cancer stem cell markers do not correlate with in vivo tumorigenicity of tumor-initiating cells.

Lehmann Christian C Jobs Gabriele G Thomas Markus M Burtscher Helmut H Kubbies Manfred M

International journal of oncology 20121005 6

The tumor-initiating capacity of primary human breast cancer cells is maintained in vitro by culturing these cells as spheres/aggregates. Inoculation of small cell numbers derived from these non-adherent cultures leads to rapid xenograft tumor formation in mice. Accordingly, injection of more differentiated monolayer cells derived from spheres results in significantly decelerated tumor growth. For our study, two breast cancer cell lines were generated from primary tumors and cultured as mammosph ...[more]

PMID: 23042145

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.

2012-12-21 | GSE32526 | GEO

Comparison of spheroid-based 3-dimensional culture to monolayer of larynx carcinoma cell line HLaC78.

Project description:In vitro proliferation and/or invasion tests (such as MTT assay, Boyden Chamber Assay, Scratch assay) using established and well-characterized cell lines can provide easy and reproducible tools to investigate anti-tumour or anti-invasion agents ex vivo. However, in vivo cells in a tissue context interact with neighbouring cells and extracellular matrix components. In 2-dimensional monolayer cultures cells tend to loose tissue-specific properties. 2-D culture models therefore seem unsuitable to mimic the behaviour of cells in a natural, 3-dimensional microenvironment, especially for testing of growth or invasion inhibiting substances. Spheroids on the other hand resemble in many aspects solid, non-vascularized tumour tissue. Within this study the larynx carcinoma cell line HLaC78 was used as a model for comparing overall gene expression in 2D monolayer culture with 72 hrs old HLaC78 multicellular spheroids, providing evidence for extensive restructuring of gene expression in the 3-dimensional context.

2016-03-11 | E-GEOD-67495 | 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

Effect of radiation and cigarette smoke on breast cells

Project description:Exposure to genotoxic stresses such as cosmic radiation and second-hand tobacco smoke may increase the risk of breast cancer formation. Towards an understanding of how exposure to these genotoxic agents affect breast cancer biogenesis, we have shown that treating non-tumorigenic immortalized breast MCF 10A cells with low doses (0.1 Gray) of radiation as well as cigarette smoke condensate can generate a neoplastic breast cancer phenotype. The transformed phenotype promoted increased mammosphere numbers, altered cell cycle phases, and increased invasion and motility. In addition, exclusion of Hoechst 33342 dye, a surrogate marker for increased ABC transporters, was observed, which indicates a possible increase in drug resistance. Furthermore, differential gene expression profiles were generated from the individual and combination treatment. Overall, the results indicate that when normal breast cells are exposed to low dose radiation in combination with cigarette smoke condensate a phenotype is generated that exhibits traits indicative of neoplastic transformation. Taken together, these results provide a new insight into a possible etiology for breast cancer formation in individuals exposed to cosmic radiation and second-hand smoke. To study the effects of low dose ionizing radiation and tobacco smoke on breast cells, MCF 10A cells were treated either with radiation (Rad - 0.1 Gray) or cigarette smoke condensate (Csc - 10 microgram/ml of medium) or a combination of Rad + Csc). Following treatments, the cells were incubated for 72 hr, RNA extracted and analyzed for differential gene expression pattern.

2010-07-07 | E-GEOD-21066 | biostudies-arrayexpress

Gene expression alteration by different cell lines derived from lung SCC of IKKM-NM-1 mutant mice

Project description:In this study, we found that kinase-dead IKKM-NM-1 knockin (KAL) mice. develop spontaneous lung squamous cell carcinomas (SCCs) associated with IKKM-NM-1 downregulation and marked pulmonary inflammation.KKM-NM-1 downregulation dysregulates the expression of multiple oncogenes and tumor suppressors in K5+ lung epithelial cells. The mutant macrophages increase inflammatory responses and oxidative stress to promote DNA damage in IKKM-NM-1-mutant K5+ lung epithelial cells, which further dysregulate the levels of multiple oncogenes, tumor suppressors, and stem cell genes, thereby promoting the IKKM-NM-1lowK5+p63hi cell transition to tumor cells in L-IkkM-NM-1KA/KA lungs. To further investigate the underlying mechanisms by which the lung SCC development, we generated two cell lines, named as S1 and S2 individually, which were derived from KAL lung SCC. The S1 cells express high level of Sca1 and exhibit tumorigenic phenotype, while the S2 cells express low level of Sca1 and exhibit less tumorigenic phenotype. The aim of this microarray assay is to identify differentially expressed genes between S1 and S2 cells, which may highlight the important genes or pathways involved in inflammation-associated lung SCC carcinogenesis. There were two cell lines were used to perform Gene chip assay with Affymetrix. The two cell lines, named as S1 and S2 individually, were derived from KAL lung SCC. The S1 cells express high level of Sca1 and exhibit tumorigenic phenotype, while the S2 cells express low level of Sca1 and exhibit less tumorigenic phenotype.

2015-01-27 | E-GEOD-65291 | biostudies-arrayexpress

Serum Conditions Do Not Abolish The Tumorigenicity of Glioma Stem Cells

Project description:The subset of GBM patient samples gives rise to adherent cultures even in sphere culture conditions. Most samples in this subset are tumorigenic and exhibit a hybrid expression profile when tested with the marker panel. Cultures from these samples have a predominantly mesenchymal character based on substrate adherence, morphology, differentiation potential and gene expression. Total RNA isolated from glioblastoma stem cells (GSC) cultured as spheres was compared to that from adherent GSCs cultured in sphere culture conditions that exhibited both GSC and mesenchymal properties.

2016-07-21 | E-GEOD-74571 | biostudies-arrayexpress

Transcription profiling by array of human prostate cancer cells enriched for cell surface markers CD44/CD133/alpha 2 beta 1 integrin

Project description:Self-renewing tumor initiating cells that are capable of differentiation and responsible for tumor growth have been isolated from cancers and cell lines. If such minor populations are associated with tumor progression, understanding molecular pathways that are required for viability and maintenance of these populations will allow to target these pathways to eradicate tumors that are resistant to existing therapies. In this study we enriched for prostate cancer progenitors (Pr. CPM-CM-"M-BM-^@M-BM-^Ys) expressing cell surface markers CD44/CD133/alpha 2 beta 1 integrin in non-adherent serum-free growth conditions maintained as spheres. Cells grown in these conditions have increased in vivo clonogenic and in vivo tumorigenic potential. microarray analysis of cells grown in sphere conditions compared with long term monolayer culture conditions revealed preferential activation of PI3K/AKT pathway in prostate cancer progenitors. PI3K p110 alpha and beta protein levels were high in sphere condition cultured cells, and PTEN knockdown lead to an increase in Pr.CPM-CM-"M-BM-^@M-BM-^Ys, and to increased clonogenic and tumorigenic potential. Inhibition of Akt1 phosphorylation target FoxO3a lead to inhibition of tumorigenic capacity in vivo for prostate cancer cells. Inhibition of PI3K activity by PI3K inhibitor NVP-BEZ235 lead to a selective inhibition of Pr.CPM-CM-"M-BM-^@M-BM-^Ys, nuclear localization of FoxO3a and increase in GADD45a in prostate cancer cells. Taken together our data strongly suggest that PTEN and PI3K/Akt pathways are critical for prostate cancer stem-like cell maintenance and targeting the PI3K signaling by selective inhibitors may give an incredible advancement in prostate cancer treatment. Experiment Overall Design: sphere and monolayer cultures from two different prostate cancer cell lines

2009-01-13 | E-GEOD-10832 | biostudies-arrayexpress

Transient treatment with epigenetic modifiers yields stable neuroblastoma stem cells resembling aggressive large-cell neuroblastomas

Project description:Cancer stem cells (CSCs) are plastic in nature, a characteristic that hampers cancer therapeutics. Neuroblastoma (NB) is a pediatric tumor of neural crest origin, and half of the cases are highly aggressive. By treating NB cell lines (SKNAS, SKNBE(2)C, CHP134, SY5Y) with epigenetic modifiers for a short time followed by sphere-forming culture conditions, we have established stem cell-like NB cells that are phenotypically stable for over a year. These cells are characterized by their high expression of stemness factors, stem cell markers, and open chromatin structure. We referred to these cells as induced CSC (iCSC). SKNAS iCSC and SKNBE(2)C iCSC clones (as few as 100 cells) injected subcutaneously into SCID/Beige mice formed tumors, and in one case, SKNBE(2)C iCSC metastasized to the adrenal gland, suggesting their increased metastatic potential. SKNAS iCSC xenografts showed the histologic appearance of totally undifferentiated “large-cell” NBs (LCNs), the most aggressive and deadly form of NB in humans. Immunohistochemical analyses showed that SKNAS iCSC xenografts expressed high levels of the stem cell marker CXCR4, while the SKNAS monolayer cell xenografts did not. The patterns of CXCR4 and MYC expression in SKNAS iCSC xenografts resembled those in the LCNs. The xenografts established from the NB iCSCs shared two common features: the LCN phenotype and high-level MYC/MYCN expression. These observations suggest that NB cells with large and vesicular nuclei, representing their open chromatin structure, are indicative of stem cell-like tumor cells, and that epigenetic changes may have contributed to the development of these most malignant NB cells. Gene expression profiles of SKNAS monolayer culture, sphere culture and iCSC culture were comparatively analyzed to examine the stem cell phenotype of each culture condition.

2013-04-02 | E-GEOD-44537 | biostudies-arrayexpress

Enhancer-associated H3K4 mono-methylation by Drosophila Trithorax-related, the Drosophila homolog of Mll3/Mll4

Project description:Mono-methylation of histone H3 on lysine 4 (H3K4me1) and acetylation of histone H3 on lysine 27 (H3K27ac) are histone modifications that are highly enriched over the body of actively transcribed genes and enhancers. Although in yeast all H3K4 methylation patterns including H3K4me1 are implemented by Set1/COMPASS, there are three classes of COMPASS-like complexes in Drosophila that could carry out H3K4me1 on enhancers: dSet1, Trithorax and Trithorax-related (Trr). Here, we report that Trr, the Drosophila homolog of mammalian Mll3/4, can function as a major H3K4 mono-methyltransferase on enhancers in vivo. Loss of Trr results in a global decrease of H3K4me1 and H3K27ac in various tissues. Assays with the cut wing margin enhancer imply a functional role for Trr in enhancer-mediated processes. A genome-wide analysis demonstrates that Trr is required for H3K4me1 and H3K27ac on chromatin signatures that resemble the histone modification patterns described for enhancers. Since Trr and mammalian Mll3/4 complexes are distinguished by bearing a unique subunit, the H3K27 demethylase UTX, we propose a model in which the H3K4 mono-methyltransferase Trr, and the H3K27 demethylase, UTX, cooperate to regulate the transition from inactive/poised to active enhancers. ChIP-seq of Trr, LPT, UTX in Drosophila S2 Cells. ChIP-seq of H3K4me1, H3K4me3, H3K27ac, H3K27me3 in WT and Trr knock-down Drosophila S2 cells. ChIP-seq of H3K4me1, H3K27me3 in LPT knock-down Drosophila S2 cells. ChIP-seq of LPT and UTX in Trr knock-down Drosophila S2 cells. ChIP-seq of H3K4me1 and H3K27me3 in MLL1(+/+), MLL1(-/-), MLL3(+/+), and MLL3(-/-) Mouse Embryonic Fibroblasts (MEFs).

2012-12-01 | E-GEOD-41440 | biostudies-arrayexpress

Gene expression alteration by different cell lines derived from lung SCC of IKKα mutant mice

Project description:In this study, we found that kinase-dead IKKα knockin (KAL) mice. develop spontaneous lung squamous cell carcinomas (SCCs) associated with IKKα downregulation and marked pulmonary inflammation.KKα downregulation dysregulates the expression of multiple oncogenes and tumor suppressors in K5+ lung epithelial cells. The mutant macrophages increase inflammatory responses and oxidative stress to promote DNA damage in IKKα-mutant K5+ lung epithelial cells, which further dysregulate the levels of multiple oncogenes, tumor suppressors, and stem cell genes, thereby promoting the IKKαlowK5+p63hi cell transition to tumor cells in L-IkkαKA/KA lungs. To further investigate the underlying mechanisms by which the lung SCC development, we generated two cell lines, named as S1 and S2 individually, which were derived from KAL lung SCC. The S1 cells express high level of Sca1 and exhibit tumorigenic phenotype, while the S2 cells express low level of Sca1 and exhibit less tumorigenic phenotype. The aim of this microarray assay is to identify differentially expressed genes between S1 and S2 cells, which may highlight the important genes or pathways involved in inflammation-associated lung SCC carcinogenesis.

2015-01-27 | GSE65291 | GEO

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