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Expression data of GFP-high or low cells of LGR5-GFP or KRT20-GFP knock-in human colorectal tumor organoids.

GSE83513 Homo sapiens (human) Expression microarray 14 samples Submitted 2017/03/30 Platform GPL15207
At a glance

Expression microarray · human · 14 samples

What it is
Expression microarrayGene activity read on a chip (the older technology that RNA-seq replaced).
Organism
Homo sapiens (human)
Topic
Colorectal cancerThis series is part of our curated briefing on it.
Samples
14 samples: 2 × CRC organoid 7 knock-in LGR5-EGFP High vs 2 × CRC organoid 7 knock-in LGR5-EGFP Low vs 2 × CRC organoid 12 knock-in LGR5-EGFP High vs 2 × CRC organoid 12 knock-in LGR5-EGFP LowGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed expression table (series matrix) and the array files, from NCBI.
Summary (written by the submitters)
We analyzed gene expression of 3 lines LGR5-GFP, 2 lines KRT20-GFP knock-in colorectal tumor organdies. The cancer stem cell (CSC) theory highlights a self-renewing subpopulation of cancer cells that fuels tumour growth. The existence of human CSCs is mainly supported by xenotransplantation of prospectively isolated cells, but their clonal dynamics and plasticity remain unclear.
Read the full summary ↓
Here, we show that human LGR5+ colorectal cancer cells serve as CSCs in growing cancer tissues. Lineage-tracing experiments with a tamoxifen inducible Cre knock-in allele of LGR5 reveal the self-renewal and differentiation capacity of LGR5+ tumour cells. Selective ablation of LGR5+ CSCs in LGR5-iCaspase9 knock-in organoids leads to tumour regression, followed by tumour regrowth driven by re-emerging LGR5+ CSCs. KRT20 knock-in reporter marks differentiated cancer cells that constantly diminish in tumour tissues, while reverting to LGR5+ CSCs and contributing to tumour regrowth after LGR5+ CSC ablation. We also show that combined chemotherapy potentiates LGR5+ CSCs targeting. These data provide insights into the plasticity of CSCs and their potential as a therapeutic target in human colorectal cancer.
This dataset
Download · which file do I need?

Direct links to NCBI, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need.

All supplementary files ↗
3 · The original raw files

Whole study · RAW.tar

Everything the authors deposited as one archive (GSE83513_RAW.tar), including the raw array or instrument files. Can be large; the picker in step 2 takes just the samples you need.

What the files usually look like: For arrays the series matrix is normally the normalised expression table you want; the raw array files (CEL and similar) are in the RAW.tar.

Also filed as BioProject PRJNA326230. Searching any of these in the dataset finder brings you back here.

Study design
2 × CRC organoid 7 knock-in LGR5-EGFP High vs 2 × CRC organoid 7 knock-in LGR5-EGFP Low vs 2 × CRC organoid 12 knock-in LGR5-EGFP High vs 2 × CRC organoid 12 knock-in LGR5-EGFP Low

Supports a between-group comparison across 8 samples.

How we read this: 4 replicated groups read from 14 sample titles; they account for 8 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
More Colorectal cancer datasets

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