Journal
NATURE
Volume 435, Issue 7045, Pages 1126-1130Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature03626
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- ICREA Funding Source: Custom
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Most sporadic colorectal cancers are initiated by activating Wnt pathway mutations(1), characterized by the stabilization of beta-catenin and constitutive transcription by the beta-catenin/T cell factor-4 (Tcf-4) complex(2,3). EphB guidance receptors are Tcf4 target genes that control intestinal epithelial architecture through repulsive interactions with Ephrin-B ligands(4,5). Here we show that, although Wnt signalling remains constitutively active, most human colorectal cancers lose expression of EphB at the adenoma-carcinoma transition. Loss of EphB expression strongly correlates with degree of malignancy. Furthermore, reduction of EphB activity accelerates tumorigenesis in the colon and rectum of Apc(Min/+) mice, and results in the formation of aggressive adenocarcinomas. Our data demonstrate that loss of EphB expression represents a critical step in colorectal cancer progression.
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