Abstract
Colon cancer is one of the leading causes of cancer-related death worldwide. Genetic changes leading to aberrant activation of APC/β-catenin/TCF (canonical Wnt) pathway are considered as the initiating step in colon cancer. Abundant studies revealed that colon cancer is “Wnt addiction” and reduced the Wnt signal is of therapeutic value. Deregulation of the Rb/E2F1 pathway, as a result of alterations in members of the pathway, is a hallmark of many human cancers, but mutations in this pathway are rare in colon cancers. In contrast, suppression of E2F1 activity through mutation of the CDK8 pathway is common in colon cancer. Active E2F1 is found to repress the activity of β-catenin transcription and promote cell apoptosis. The mutually exclusive expression pattern and function between E2F1 and Wnt pathway suggest an antagonistic relationship between these two pathways in colon cancer evolution. We hypothesize that E2F1 functions as a barrier of aberrant Wnt signal, and that E2F1 repression is necessary for colon cancer development. This hypothesis suggests that reactivation of E2F1 might have therapeutic potential for most of the colon cancers, as most of the colon cancers have aberrantly activated Wnt signal.
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