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ShareJune 10, 2008 — A team of scientists at the Genome Institute of Singapore (GIS), a research institute of the Asian city-state's Agency for Science, Technology and Research (A*STAR), and the University of California at San Francisco have developed a pharmacological approach to kill colon cancer cells.
Genetic and epigenetic defects in the signaling of a protein called Wnt/²-catenin, which is often found to be abnormally activated in human malignance, play important roles in colorectal cancer development. The team of scientists identified a gene, called DACT3, whose function is to inhibit Wnt/²-catenin, is often lost (or transcriptionally silenced) in colorectal cancer.
Apart from the findings on DACT3, they have also developed a pharmacological approach to restore the expression of DACT3, which results in the effective inhibition of Wnt/²-catenin massive death of colon cancer cells.
GIS Group Leader, Yu Qiang, Ph.D., said, "This work identifies a significant new regulator of the Wnt/²-catenin avenue for future colorectal cancer research."
Edison Liu, M.D., Executive Director of GIS, added, "This is indeed a very significant discovery. It suggests a novel therapy for colorectal cancer, an important step towards clinical treatment for the disease, which is one of the leading causes of death from tumours."
The team is now working with other A*STAR research institutes and industry partners for the development of potential drug candidates based on this technology.
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The above story is reprinted from materials provided by Agency for Science, Technology and Research (A*STAR), Singapore.
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Journal Reference:
- Xia Jiang et al. DACT3 is an epigenetic regulator of Wnt/%u03B2-catenin signaling in colorectal cancer and is a therapeutic target of histone modifications. Cancer Cell, June 9, 2008
Note: If no author is given, the source is cited instead.
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