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Home › Dataset Library › Expression data from subpopulations of Apc1638N/+ intestinal adeno tumors versus Apc1638N/+ / KRAS v12G intestinal adenocarcinomas tumors

Dataset: Expression data from subpopulations of Apc1638N/+ intestinal adeno tumors versus Apc1638N/+ / KRAS v12G intestinal adenocarcinomas tumors

Constitutive activation of the Wnt pathway leads to adenoma formation, an obligatory step towards intestinal cancer. In view of the...

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Constitutive activation of the Wnt pathway leads to adenoma formation, an obligatory step towards intestinal cancer. In view of the established role of Wnt in regulating stemness, we attempted the isolation of cancer stem cells (CSCs) from Apc- and Apc/KRAS-mutant intestinal tumours. Whereas CSCs are present in malignant Apc/KRAS–mutant carcinomas, they appear to be very rare (<10-6) in the benign Apc–mutant adenomas. In contrast, the Lin-CD24hiCD29+ subpopulation of adenocarcinoma cells appear to be enriched in CSCs with increased levels of active -catenin. Expression profiling analysis of the CSC-enriched subpopulation confirmed their enhanced Wnt activity and revealed additional differential expression of other signalling pathways, growth factor binding proteins, and extracellular matrix components. As expected, genes characteristic of the Paneth cell lineage (e.g. defensins) are co-expressed together with stem cell genes (e.g. Lgr5) within the CSC-enriched subpopulation. This is of interest as it may indicate a cancer stem cell niche role for tumor-derived Paneth-like cells, similar to their role in supporting Lgr5+ stem cells in the normal intestinal crypt. Overall, our results indicate that oncogenic KRAS activation in Apc-driven tumours results in the expansion of the CSCs compartment by increasing b-catenin intracellular stabilization. To identify molecular differences between stem-like and more differentiated (bulk) tumour cells from Apc1638N/+ and Apc1638N/+/KRASV12G intestinal adenomas and adenocarcinomas, we isolated total RNA from 104 Lin-CD24hiCD29+, Lin-CD24medCD29+/Lin-CD24loCD29+ and Lin- (bulk) tumour cells from 5 individual mice of each genotype (Apc1638N/+ and Apc1638N/+/KRASV12G). Total RNA samples were then employed to hybridize oligonucleotide microarrays (Affymetrix Mouse Genome 430A 2.0 Array) according to conventional protocols.

Species:
mouse

Samples:
24

Source:
E-GEOD-47772

Updated:
Dec.12, 2014

Registered:
Nov.12, 2014


Factors: (via ArrayExpress)
Sample TISSUE TYPE GENOTYPE
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM1156774 intestinal adeno tumor Apc1638N/+
GSM1156774 intestinal adeno tumor Apc1638N/+
GSM1156774 intestinal adeno tumor Apc1638N/+
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM115677 intestinal adenocarcinoma tumor Apc1638N/+/KRASV12G
GSM1156774 intestinal adeno tumor Apc1638N/+
GSM1156774 intestinal adeno tumor Apc1638N/+
GSM1156774 intestinal adeno tumor Apc1638N/+
GSM1156774 intestinal adeno tumor Apc1638N/+
GSM1156774 intestinal adeno tumor Apc1638N/+
GSM1156774 intestinal adeno tumor Apc1638N/+

Tags

  • adenocarcinoma
  • adenoma
  • cancer
  • cell
  • compartment
  • genome
  • intestinal cancer
  • paneth cell
  • stem cell

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