Study in Cancer Cell found that this gene inhibits the beta-catenin/TCF4 complex leading to tumor development.
The absence or inactivation of the RUNX3 gene leads to the development of colon cancer, report a group of scientists from Singapore. Using human tissue samples and animal models, they observed that inactivation of RUNX3 occurs at a very early stage of colon cancer.
Prior to these findings, scientists knew that a tumor suppressor gene called APC is disrupted in most cases of human colon cancer. APC disruption activates beta-catenin and TCF4, a protein complex that plays an important role in cancer development.
These latest findings show that RUNX3 also inhibits the activity of beta-catenin/TCF4. The current research thus demonstrates how RUNX3 acts as a tumor suppressor, which was previously discovered by the same group of investigators. RUNX3 has already been implicated in gastric, breast, lung, and bladder cancers.
The scientists point out that the inactivation of RUNX3 is relatively easy to detect, and it is possible that inactivated RUNX3 can be reactivated.
The Singapore scientists are based at the National University of Singapore’s Yong Loo Lin School of Medicine and the Institute of Molecular and Cell Biology. Their results are published in the September issue of the journal Cancer Cell.
