Abstract
The majority of human colorectal cancers have elevated β-catenin/TCF regulated transcription due to either inactivating mutations of the APC tumor suppressor gene or activating mutations of β-catenin. Surprisingly, one commonly used colorectal cancer cell line was found to have intact APC and β-catenin and no demonstrable β-catenin/TCF regulated transcription. However, this line did possess a truncating mutation in one allele of CDX2, a gene whose inactivation has recently been shown to cause colon tumorigenesis in mice. Expression of CDX2 was found to be induced by restoring expression of wild type APC in a colorectal cancer cell line. These findings raise the intriguing possibility that CDX2 contributes to APC's tumor suppressive effects.
Original language | English (US) |
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Pages (from-to) | 5010-5014 |
Number of pages | 5 |
Journal | Oncogene |
Volume | 18 |
Issue number | 35 |
DOIs | |
State | Published - Sep 2 1999 |
Keywords
- APC
- CDX2
- Colorectal cancer
- Mutation
- Regulation
ASJC Scopus subject areas
- Molecular Biology
- Genetics
- Cancer Research