Enhancement of GLI1-transcriptional activity by β-catenin in human cancer cells
Affiliations: Department of Gastroenterology, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8550, Japan
- Published online on: July 1, 2006 https://doi.org/10.3892/or.16.1.91
- Pages: 91-96
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The Hedgehog (Hh) signaling pathway and the Wnt signaling pathway are known to play important roles in carcinogenesis and the progression of various human malignant tumors. Although a relationship between these two pathways has recently been reported, the mechanism by which β-catenin, one of the key molecules of the Wnt signaling pathway, influences the Hh pathway has not yet been revealed in detail. To clarify the role of β-catenin in relation to the Hh signaling pathway, we transfected GLI1 and β-catenin expression constructs into human malignant cells, including stomach, colon, and lung cancers, and evaluated the luciferase activity of GLI-responsive reporter constructs. While exogenous GLI1 increased the luciferase activity, exogenous β-catenin also enhanced the activity under overexpression of GLI1. However, co-transfection with T-cell factor (TCF)-4 or lymphocyte enhancer factor (LEF)-1 did not influence the activity, indicating that the enhancement of β-catenin in relation to the Hh signaling pathway is not TCF/LEF-dependent. Our results suggest that β-catenin might be involved in the Hh signaling pathway via enhancement of the transcriptional activity of GLI.