A gene called TCF7L2, which was previously believed to promote colorectal cancer actually suppresses the growth of human cancer cells, scientists at UT Southwestern Medical Center have found.
"This finding reshapes a fundamental model of how colorectal cancer arises," said Dr. Lawrence Lum, assistant professor of cell biology at UT Southwestern and senior author of the study, which appears online today and in a future issue of the Proceedings of the National Academy of Sciences.The researchers set out to identify genes that contributed to a biochemical malfunction that arises from mutations in the TCF7L2 gene, and accounts for about 90 per cent of colorectal cancers.
They used the genetic screening approach RNAi mediated interference for the purpose.
The researchers employed more than 80,000 small snippets of chemically synthesized RNAs (ribonucleic acids) known as "small interfering RNAs (siRNAs)," which are each capable of inactivating a specific gene.
The researchers mixed the siRNAs with specially engineered human cancer cells that glowed when the cancer-causing malfunction was activated.
When an siRNA made a cell glow, the researchers were able to flag the gene as a candidate cancer gene.
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When the researchers inactivated the gene, human colorectal cancer cells grew more rapidly in culture and emitted a stronger glow.
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The researchers say that the next step is to gain a better understanding of all the steps in the biochemical pathway involved in controlling the action of TCF7L2, which may in turn help identify new therapeutic targets for treating colorectal cancer.
Dr. Lum believes that therapeutic strategies derived from such studies may also be useful in treating type II diabetes, for which risk is strongly associated with mutations in TCF7L2.
Source-ANI
RAS/L