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Related Experiment Videos

beta-Catenin/TCF/LEF regulate expression of the short form human Cripto-1.

Shin Hamada1, Kazuhide Watanabe, Morihisa Hirota

  • 1Mammary Biology and Tumorigenesis Laboratory, NCI/CCR, 37 Convent Drive, Building 37, Bethesda, MD 20892, USA.

Biochemical and Biophysical Research Communications
|February 13, 2007
PubMed
Summary

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The Wnt signaling pathway directly regulates the short form of Teratocarcinoma-derived growth factor 1 (TDGF1)/Cripto-1 (CR-1) expression in cancer. This regulation occurs via an enhancer element within the CR-1 gene, impacting colon cancer and hepatoma.

Area of Science:

  • Molecular biology
  • Cancer research
  • Gene regulation

Background:

  • Teratocarcinoma-derived growth factor 1 (TDGF1)/Cripto-1 (CR-1) is part of the EGF-cripto FRL1 cryptic (EGF-CFC) gene family and is expressed in various human carcinomas.
  • A constitutively active Wnt/beta-catenin/TCF signaling pathway is prevalent in colorectal tumors and hepatomas, which also express CR-1.

Purpose of the Study:

  • To investigate the potential differential regulation of CR-1 expression by the canonical Wnt signaling pathway in colon cancer and hepatoma cell lines.
  • To elucidate the mechanism of CR-1 regulation by the Wnt pathway.

Main Methods:

  • Analysis of CR-1 mRNA expression in colon carcinoma and hepatoma cell lines.
  • Identification and characterization of regulatory elements within the CR-1 gene.

Related Experiment Videos

  • Demonstration of direct transcriptional regulation by the Wnt signaling pathway.

    • Main Results:

    • The study demonstrates direct transcriptional regulation of short-form CR-1 mRNA expression by the canonical Wnt signaling pathway.
    • This regulation is mediated by an intronic-exonic enhancer element within the CR-1 gene.
    • This enhancer contains three tandem TCF/LEF binding sites, crucial for Wnt pathway-mediated regulation.

    Conclusions:

    • The canonical Wnt signaling pathway directly controls the expression of short-form CR-1.
    • The identified enhancer element is a key mediator of this regulation in cancer contexts like colon cancer and hepatoma.
    • Findings provide insights into the molecular mechanisms underlying CR-1 dysregulation in specific cancers.