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Status |
Public on Nov 02, 2012 |
Title |
COLO320 cells: siCDX2 vs. non-targeting control |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by array
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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 b-catenin transcriptional activity. These data characterize CDX2 as a novel lineage-survival oncogene deregulated in colorectal cancer.
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Overall design |
Two-condition experiment, CDX2 siRNA knockdown vs. control, using two independent siRNAs against CDX2
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Contributor(s) |
Salari K, Pollack JR |
Citation(s) |
23112155 |
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Submission date |
Jun 23, 2011 |
Last update date |
Feb 22, 2018 |
Contact name |
Keyan Salari |
E-mail(s) |
ksalari@mgh.harvard.edu
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Organization name |
Massachusetts General Hospital
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Street address |
Gray/Bigelow Rm 1102, 55 Fruit Street
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City |
Boston |
State/province |
MA |
ZIP/Postal code |
02114 |
Country |
USA |
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Platforms (1) |
GPL4133 |
Agilent-014850 Whole Human Genome Microarray 4x44K G4112F (Feature Number version) |
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Samples (2) |
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This SubSeries is part of SuperSeries: |
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Relations |
BioProject |
PRJNA155087 |