Researchers at the Charité Comprehensive Cancer Center (Berlin, Germany) and the US National Cancer Institute (NCI; Frederick, MD, USA) showed in a study from 2005 that the S100A4 gene is regulated by the cellular adhesion gene beta-catenin. When mutated, the beta-catenin gene activates the S100A4 gene, thus triggering colon cancer metastasis. To identify a transcription inhibitor of S100A4, high-throughput screening of 1,280 pharmacologically active compounds was performed using a human colon cancer-cell line expressing a luciferase (LUC) reporter gene construct.
The researchers found that niclosamide, a drug currently approved by the US Food and Drug Administration (FDA) to treat intestinal parasite infections, was a good candidate. Niclosamide reduced S100A4 mRNA and protein expression, and inhibited cell migration, invasion, proliferation, and colony formation. In vivo imaging showed reduced liver metastasis compared with solvent-treated control mice. Compared with the control group, discontinuation of treatment for 26 days showed reduced liver metastasis formation in mice and increased overall survival. The researchers concluded that niclosamide inhibits S100A4-induced metastasis formation and has therapeutic potential. The study was published ahead of print on June 17, 2011, in the Journal of the National Cancer Institute.
Niclosamide is a teniacide in the anthelmintic family especially effective against cestodes that infect humans; it is also used as a piscicide. But while antihelmintics are a drug family used to treat worm infections, niclosamide is used specifically to treat tapeworms and is not effective against worms such as pinworms or roundworms. It is a chewable tablet taken orally, dosage depending on type of worm and the patient's age and/or weight.
Related Links:
Charité Comprehensive Cancer Center
US National Cancer Institute (NC)
