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Gene expression in colon cancer stem cells (CSC) cultures identified by Wnt signaling levels

ABSTRACT: Primary colon CSC cultures were transduced with a Wnt responsive construct (TOP-GFP). 10% highest and lowest TOP-GFP cell fractions were FACS sorted and arrayed.

ORGANISM(S): Homo sapiens

PROVIDER: GSE33112 | GEO | 2011/11/05

SECONDARY ACCESSION(S): PRJNA156583

REPOSITORIES: GEO

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Gene expression in colon cancer stem cells (CSC) cultures identified by Wnt signaling levels

Project description:Primary colon CSC cultures were transduced with a Wnt responsive construct (TOP-GFP). 10% highest and lowest TOP-GFP cell fractions were FACS sorted and arrayed. Primary colon CSC cultures with a responsive construct (TOP-GFP): high and low TOP-GFP cell fractions. 12 samples.

2011-11-05 | E-GEOD-33112 | biostudies-arrayexpress

Gene expression in colon cancer stem cells (CSC) cultures identified by Wnt signaling levels

2009-12-01 | GSE17375 | GEO

Gene expression in colon cancer stem cells (CSC) cultures identified by Wnt signaling levels

Project description:Primary colon CSC cultures were transduced with a Wnt responsive construct (TOP-GFP) and were single cell cloned. 10% highest and lowest TOP-GFP cell fractions were FACS sorted and arrayed. Primary colon CSC cultures with a responsive construct (TOP-GFP): high and low TOP-GFP cell fractions. 4 samples.

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Transcriptome profiling of CD44highCD24low(CSC) and CD44lowCD24high(Non-CSC) SCC25 cells

Project description:In the present study, we have characterized the putative Cancer Stem Cell population of Oral Squamous Cell Carcinoma by various cellular and molecular assay. Subsequently we performed gene expression profiling of SCC25 cell line with CD44highCD24low(CSC) and CD44lowCD24high(Non-CSC) phenotypes using illumina BeadChip Array. Further, systematic computational analysis was performed to identify CSC-like gene signatures in the oral cancer cells. Differentially expressed genes were subjected to pathway analysis in IPA. The analysis lead to the identification of few relevant signaling pathway implicated in stemness.

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Expression data from CSC and Non-CSC of three HCC cell lines

Project description:Hepatocellular carcinoma (HCC) represents the major subtype of liver cancer, characterized with a high rate of recurrence and heterogeneity. Liver cancer stem cells (CSCs) may account for a hierarchical organization of heterogeneous cancer cells. However, how liver CSCs sustain their self-renewal remains largely unknown. We used microarrays to discover the long non-coding RNAs (lncRNAs) expression underlying cell stem cell (CSC) and non cell stem cell (non-CSC) and identified distinct lncRNAs during this process. We sorted CD13+CD133+ and CD13-CD133- cells from Hep3B, Huh7, and PLC/PRF/5 HCC cell lines as liver CSCs and non-CSCs, then hybridized on Affymetrix microarrays. We sought to identify distinct lncRNAs in liver CSCs.

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Expression data from CSC and Non-CSC of three primary HCC samples

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Gene expression profiling along the intestinal crypt axis.

Project description:The identification of Lgr5 as an intestinal stem cell marker has made it possible to isolate and study primary intestinal stem cells. Transcriptional differences between intestinal stem cells can be explored by the use of the Lgr5-eGFP-ires-CreERT2 knock-in mouse. In this mouse model GFP expression is driven from the Lgr5 locus, leading to highest GFP levels in the Lgr5 positive cells. Yet, due to the stability of the GFP protein, it is distributed upon cell division to the daughter cells. Here we arbitrarily sorted crypt cells based on GFP expression into five fractions. The fraction with the lowest GFP level is named 1+, the fraction with the highest level 5+. We used cell fractions of intestines from Lgr5-EGFP-ires-CreERT2 mice, expressing GFP under the control of the Lgr5 promoter. RNA was isolated from five FACS sorted cell populations, with fraction 5+ expressing GFP at highest levels and 1+ expressing GFP at lowest levels. Differentially labelled cRNA from fractions 1+ to 4+ were hybridized against fraction 5+ on 4X44K Agilent Whole Mouse Genome dual colour Microarrays (G4122F) in dye swap experiments, resulting in eight individual arrays.

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Genome-wide analysis of gene expression by IFNβ in Transformed HMEC (Epithelial/non-CSC, Mesenchymal/CSC)

Project description:Triple Negative Breast Cancer (TNBC), the deadliest form of this disease, lacks a targeted therapy. TNBC tumors that fail to respond to chemotherapy are characterized by a repressed Interferon/Signal Transducer and Activator of Transcription (IFN/STAT) gene signature and are often enriched for Cancer Stem Cells (CSCs). We have found that human mammary epithelial cells that undergo an Epithelial-to-Mesenchymal Transition (EMT) following transformation acquire CSC properties. These mesenchymal/CSCs have a significantly repressed IFN/STAT gene expression signature and an enhanced ability to migrate and form tumor spheres. Treatment with Interferon-Beta (IFNb) led to a less aggressive epithelial/non-CSC-like state, with repressed expression of mesenchymal proteins (VIMENTIN, SLUG), reduced migration and tumor sphere formation, and re-expression of CD24 (a surface marker for non-CSCs), concomitant with an epithelial-like morphology. The CSC-like properties were correlated with high levels of unphosphorylated Interferon Stimulated Gene Factor 3 (U-ISGF3), which was previously linked to resistance to DNA damage. Inhibiting the expression of IRF9 (the DNA-binding component of U-ISGF3) reduced the migration of mesenchymal/CSCs. Here we report a positive translational role for IFNb as gene expression profiling of patient derived TNBC tumors demonstrates that an IFNb Metagene signature correlates with improved patient survival, an immune response linked with Tumor Infiltrating Lymphocytes (TILs) and a repressed CSC Metagene signature. Taken together, our findings indicate that repressed IFN signaling in TNBCs with CSC-like properties is due to high levels of U-ISGF3, and that treatment with IFNb reduces CSC properties, suggesting a novel therapeutic strategy to treat drug-resistant, highly aggressive TNBC tumors.

2017-11-12 | GSE106782 | GEO

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