The gene CDK8, which was believed to be harmless, has now been proved to be linked to colon cancer. The research was conducted by the Dana-Farber Cancer Institute, Boston, USA.
The scientists identified the CDK8 gene with the help of new tools they had developed for assessing the activity of specific genes.
They suggest that as the tools improve, the stream of newly discovered cancer genes is expected to increase, providing new avenues for therapy.
"This study provides confirmation that many of the genes involved in cancer have yet to be identified," Nature magazine quoted study's senior author, Dr. William Hahn, of Dana-Farber and the Broad Institute of Harvard and M.I.T, as saying.
"When it comes to identifying gene targets for therapy, we've really only scratched the surface," he added.
According to the researchers, many of the abnormal proteins associated with cancer are known as "transcription factors" because they are able to "read" cell DNA, and use that information for producing other cell proteins.
Though such proteins cannot be targeted with drugs, genes that affect such transcription factors can be potential targets for drugs.
CDK8 is one such gene, say the researchers.
During the study, the researchers focused on a protein called beta-catenin, a transcription factor that is overactive in nearly all colorectal cancers.
They tried to determine which genes control the production of beta-catenin, and are involved in the proliferation of colon cancer cells.
They conducted three screening tests. In the first two tests, the researchers used RNA interference to turn off more than a thousand genes one by one and recorded the instances where beta-catenin activity decreased and the cells stopped growing. They later analyzed colon cancers for genes that had extra copies.
Hahn said that the results of the three tests overlapped, one gene stood out CDK8.
He said that the protein produced from CDK8 is part of the "mediator complex", a collection of proteins that serves as a bridge for compounds involved in gene transcription.
"This study demonstrates that blocking CDK8 interferes with the proliferation of colon cancer cells that have high levels of the CDK8 protein and overactive beta-catenin," said Hahn.
"Drugs that target CDK8 may be very useful against tumors whose growth is driven by beta-catenin," he added.