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Status |
Public on Mar 15, 2011 |
Title |
Gene expression in Tcf4Het ApcHet mouse colon tumors compared to normal colon |
Organism |
Mus musculus |
Experiment type |
Expression profiling by array
|
Summary |
The Wnt/β-catenin pathway plays multiple/diverse roles in development by regulating gene expression via Tcf/Lef DNA binding factors. Misregulation of this pathway is thought to initiate colon adenoma formation. It is controversial whether Tcf4 (Tcf7L2) functions as an oncogene or tumor suppressor gene in colon carcinogenesis. We show here that Tcf4 haploinsufficiency results in colon tumor formation in a mouse tumor model that normally only develops small intestinal tumors. Further, we show that loss of Tcf4 early in development and in adult colon results in increased cell proliferation. These findings strongly suggest that Tcf4 normally modulates proliferation of the colonic epithelium and that disruption of Tcf4 activity increases proliferation leading to colon tumorigenesis. Taken together our in vivo studies favor a tumor suppressor function for Tcf4.
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Overall design |
4 Normal Colon and 4 colon tumor from independent mouse tissue samples
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Contributor(s) |
Capecchi MR, Angus-Hill ML |
Citation(s) |
21383188 |
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Submission date |
Feb 25, 2011 |
Last update date |
Jan 12, 2017 |
Contact name |
Mario R. Capecchi |
Organization name |
University of Utah
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Street address |
15 North 2030 East
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City |
Salt Lake City |
State/province |
UT |
ZIP/Postal code |
84112 |
Country |
USA |
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Platforms (1) |
GPL7202 |
Agilent-014868 Whole Mouse Genome Microarray 4x44K G4122F (Probe Name version) |
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Samples (8)
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Relations |
BioProject |
PRJNA137107 |