Transcriptomes of adult sorted Epcam+ CD44- enterocytes from small intestine of wildtype and CmafLEC-KO mice
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ABSTRACT:
PROVIDER: PRJNA784785 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17073217_1.fastq.gz | Fastqsanger.gz | |||
| SRR17073217_2.fastq.gz | Fastqsanger.gz | |||
| SRR17073218_1.fastq.gz | Fastqsanger.gz | |||
| SRR17073218_2.fastq.gz | Fastqsanger.gz | |||
| SRR17073219_1.fastq.gz | Fastqsanger.gz |
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Project description:In human colon cancer, the malignant component of tumor tissues often contains multiple sub-types of cancer cells, whose transcriptional profiles and surface marker phenotypes correspond to those of the epithelial lineages that are found in normal colonic crypts (e.g., goblet cells, enterocytes, LGR5+ columnar basal cells). Among those various sub-types of malignant cells, those characterized by a surface marker phenotype that is characteristic of epithelial stem/progenitor cells residing at the bottom of colonic crypts (EpCAM+, CD44+, CD166+) are enriched in cells with "cancer stem cell" (CSC) properties, such as self-renewal (i.e., the capacity to sustain the formation of new tumors upon serial xeno-transplantation in immune-deficient animals) and multi-lineage differentiation (i.e., the capacity to sustain the formation of other cell-types, thus reconstituting the heterogeneous population of the parent tumors from which they have been isolated). Cell populations with "cancer stem cell" (CSC) properties are known to be preferentially resistant to several cytotoxic agents used in conventional chemotherapy, but the molecular mechanisms underpinning this property remain poorly understood. In this dataset, we report the analysis by gene-expression microarrays of the transcriptional profile of two sub-populations of human colon cancer cells: 1) cells with a "bottom-of-the-crypt" phenotype (EpCAM+, CD44+, CD166+), which are known to be enriched in "cancer stem cells" (CSCs); and 2) cells with a "top-of-the-crypt" phenotype (EpCAM+, CD44neg, CD166neg), which are known to be non-tumorigenic upon xeno-transplantation in immune-deficient mice. The two populations were purified in parallel by fluorescence activated cell sorting (FACS), starting from solid tumors established by sub-cutaneous (s.c.) engraftment in immune-deficient mice of a patient-derived xenograft (PDX) line representative of a moderately differentiated (G2) primary colon carcinoma. To identify genes whose expression is modulated by in vivo exposure to chemotherapy (and thus potentially involved in the mechanistic regulation of chemo-resistance), we compared the transcriptional profile of cells purified from tumors that were exposed to 4 weeks of in vivo treatment with either irinotecan (CPT-11) or a placebo control (saline solution).
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Project description:Targeted therapies against cancer stem cells which are enriched in side populations (SP) involves interruption of Wnt-signalling. Furthermore, EpCAM is a SP marker and modulator of Wnt-signalling. Therefore, the effects of an anti-EpCAM treatment on SP-cells and WNT/β-catenin signalling was studied. SP of the human lung adenocarcinoma cell line A549 was obtained by fluorescence activated cell sorting and whole genome scans helped to define their molecular phenotype after anti-EpCAM antibody treatment.
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Project description:Tumorigenic breast cancer cells characterized by CD44 expression and low or undetectable CD24 levels (CD44+/CD24-/low) may be resistant to chemotherapy and therefore responsible for cancer relapse. Paired breast cancer core biopsies before and after neoadjuvant chemotherapy or lapatinib were obtained and as single cell suspensions stained using antibodies against CD24, CD44, and lineage markers, and then analyzed by flow cytometry. Mammosphere (MS) formation in culture was compared before and after treatment. Global gene expression differences between cancer cells bearing CD44+/CD24-/low cells and all other sorted cells, and between cancer MS and the primary bulk invasive cancers were analyzed. We report that CD44+/CD24-/low tumorigenic breast cancer cells were intrinsically chemoresistant â chemotherapy led to increased CD44+/CD24-/low cells, increased self-renewal capacity on MS assays, and enhanced tumorigeneicity in immunocompromised SCID/Beige mice. Conversely, in patients with HER2 overexpressing tumors, the EGFR/HER2 tyrosine kinase inhibitor, lapatinib decreased CD44+/CD24-/low cells, with the majority of these patients after conventional therapy achieving pathologic complete response, a validated surrogate marker for long-term survival. Gene transcription pathways that underlie chemoresistant, MS-forming CD44+/CD24-/low cells involve genes belonging to stem cell self-renewal, Wnt signaling, and early development pathways. Experiment Overall Design: Human breast tumor samples were sorted using flow cytometry to select for cells that were CD44+ and CD24-. Gene expression profiles of these cells were compared with profiles of the other sorted cells (CD24+ and CD44-/CD24-). Experiment Overall Design: Core biopsies of primary breast tumors were taken and placed immediately in cold RPMI-1640 supplemented with 10% heat-inactivated newborn calf serum (HINCS, Invitrogen, Carlsbad, CA). Within an hour, the samples were minced and then digested in 10-15 mL of MEGM with 250-300 units/mL collagenase at 370C. The samples were filtered, washed, and then subjected to hypotonic shock to lyse red blood cells. About 106 single cells were re-suspended, incubated for 15 min at 40C with anti-CD44 (APC), anti-CD24 (FITC), and anti-lineage cocktail antibodies (PE-conjugated anti-CD2, CD3, CD10, CD16, CD18, CD31 and CD 140B) (Pharmingen, San Diego, CA) using the manufacturerâs suggested concentrations. The cells were then washed twice, re-suspended with the viability dye propidium iodide, and analyzed using Dako MoFlo flow cytometry. Side- and forward- scatter were used to eliminate debris and cell doublets, and the Lin- cells were further analyzed by CD44 and CD24 markers.
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2012-08-07 | E-GEOD-31315 | biostudies-arrayexpress
Project description:Targeted therapies against cancer stem cells which are enriched in side populations (SP) involves interruption of Wnt-signalling. Furthermore, EpCAM is a SP marker and modulator of Wnt-signalling. Therefore, the effects of an anti-EpCAM treatment on SP-cells and WNT/M-NM-2-catenin signalling was studied. SP of the murine lung adenocarcinoma cell line A2C12 was obtained by fluorescence activated cell sorting and whole genome scans helped to define their molecular phenotype after anti-EpCAM antibody treatment. Anti-EpCAM treated and untreated A2C12 cells were subjected to Hoechst 33342 dye exclusion assay and sorted to SP and non-SP fractions by FACS. Three biological replicates.
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