- U. Sack
- U. Stein
- General Physiology and Biophysics
- Gen Physiol Biophys 28 (Focus Iss): F55-F64
Colon cancer is still a burden mainly due to metastasis formation. The latter is often associated with a constitutive activation of the Wnt/beta-catenin signaling pathway and high expression of the metastasis-inducing gene S100A4. We previously identified S100A4 as a transcriptional target of beta-catenin. Intervention strategies targeting Wnt/beta-catenin signaling might therefore represent promising approaches to inhibit tumor growth and metastasis formation when induced by S100A4. Many inhibitors, various strategies, as well as different routes of application targeting key molecules of the Wnt signaling pathway have been reported within the last decade. Consequently, downregulation of beta-catenin target genes lead to altered tumorigenic and metastastic abilities of cancer cells. This review focuses on the potential of Wnt/beta-catenin signaling intervention to restrict colon cancer metastasis formation by interdicting S100A4 expression.