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Singapore research team develops new strategy on inflammation cancer targeting
Drug Discovery
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SINGAPORE–A research team at the National University of Singapore (NUS) has published a paper on a novel strategy to prevent progression of inflammation-associated cancers that targets the specific pathological function of the “culprit” molecule rather than inhibiting its gene expression, according to a Feb. 13 news release.

The findings were published in the Proceedings of the National Academy of Sciences (PNAS) on Nov. 24, 2014.

Led by Associate Professor Caroline Lee from the Yong Loo Lin School of Medicine at the National University of Singapore, in collaboration with Associate Professor Song Jianxing of the Department of Biological Sciences at the NUS Faculty of Science, they discovered that the interaction between two proteins, namely FAT10 and MAD2, leads to inflammation-associated cancers, such as liver (hepatocellular carcinoma) and colorectal cancers, according to the news release.

A disruption of this unique interaction can prevent cancer, according to the authors, possibly paving the way to design drugs that target the specific interaction without affecting other important cellular functions of the molecule that causes cancer, thereby minimizing undesirable side effects.

FAT10 is a protein that is expressed mainly in tissues of the immune system, including the spleen and thymus.

In their previous studies, Lee, who also holds joint appointments at Duke-NUS Graduate Medical School and the National Cancer Centre Singapore, and her team had found that overexpression of FAT10 promotes tumor formation, growth and progression.

The researchers determined the three-dimensional structures of FAT10 using the state-of-the-art nuclear magnetic resonance (NMR) spectroscopy, and further examined the relationship between the two proteins.

“Many current strategies target over-expressed genes to inhibit their expression,” Lee said in the release.

“Our strategy works differently as it targets a specific pathological function of the ‘culprit’ molecule without affecting its other physiological functions. This is especially important for a molecule like FAT10 which is not only over-expressed during cancer formation but is also over-expressed during immune response.”



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