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| Status |
Public on Nov 02, 2012 |
| Title |
CDX2 ChIP-seq |
| Organism |
Homo sapiens |
| Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
|
| Summary |
Somatic DNA alteration underlies tumor development and progression, and gives rise to tumors with diverse genetic contexts. Here, we identify in a collection of 29 colorectal cancer cell lines and 226 primary colorectal tumors recurrent amplification of chromosome 13, an alteration highly restricted to colorectal-derived cancers. A minimal region of amplification on 13q12.2 pinpoints caudal type homeobox transcription factor CDX2, a master regulator of anterior-posterior patterning, midgut development, and intestinal epithelial cell differentiation and maintenance. In contrast to its described role as a colorectal tumor suppressor, we show that in the context of genomic amplification, CDX2 is required for proliferation and anchorage-independent growth of colorectal cancer cells. By genome-wide expression and location analysis, we reveal that CDX2 directly promotes expression of Wnt pathway genes. Further results suggest that CDX2 induces expression of intestinal differentiation markers and modulates β-catenin transcriptional activity. These data characterize CDX2 as a novel lineage-survival oncogene deregulated in colorectal cancer.
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| |
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| Overall design |
ChIP-seq analysis of CDX2 binding sites in COLO320 cells
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| Contributor(s) |
Salari K, Pollack JR |
| Citation(s) |
23112155 |
| Submission date |
Jun 16, 2011 |
| Last update date |
May 15, 2019 |
| Contact name |
Keyan Salari |
| E-mail(s) |
ksalari@mgh.harvard.edu
|
| Organization name |
Massachusetts General Hospital
|
| Street address |
Gray/Bigelow Rm 1102, 55 Fruit Street
|
| City |
Boston |
| State/province |
MA |
| ZIP/Postal code |
02114 |
| Country |
USA |
| |
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| Platforms (1) |
| GPL10999 |
Illumina Genome Analyzer IIx (Homo sapiens) |
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| Samples (3) |
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| This SubSeries is part of SuperSeries: |
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| Relations |
| SRA |
SRP007215 |
| BioProject |
PRJNA155363 |
