The absence or inactivation of the RUNX3 gatekeeper gene paves the way for the growth and development of colon cancer, Singapore scientists report in the Sept. issue of the journal Cancer Cell. Previous studies have shown that RUNX3 plays a role in gastric, breast, lung and bladder cancers.
The inactivation of RUNX3 occurs at a very early stage of colon cancer, according to the Singapore scientists' studies with human tissue samples and animal models.
Because the inactivation of RUNX3 is relatively easy to detect, and it is possible that inactivated RUNX3 can be reactivated, this new research may prove to be a crucial step in the development of an early diagnostic test as well as a therapeutic target for colon cancer.
Prior to these new findings, scientists knew that a tumor suppressor gene called APC is disrupted in most cases of human colon cancer. APC disruption activates bete-catenin and TCF4, a protein complex that plays an important role in cancer development. For decades, this has been considered the molecular basis for colon cancer.
These latest findings are the first to show that the activity of beta- catenin/TCF4 also is inhibited by RUNX3.
The Singapore scientists are based at the National University of Singapore's (NUS) Yong Loo Lin School of Medicine and the Institute of Molecular and Cell Biology (IMCB), one of the 14 research institutes under the country's Agency for Science, Technology and Research (A*STAR).
In an earlier research, the same team of researchers reported that RUNX3 is a major tumor suppressor of gastric cancer.
Leading the Singapore team is Yoshiaki Ito, M.D., NUS Yong Loo Lin Professor in Medical Oncology and a principal investigator at IMCB.
In their latest study, supported by A*STAR, Dr. Ito and his team analyzed animal models as well as tissue samples from patients diagnosed with colon cancer, with prior ethical approval obtained from the Insti
|Contact: Cathy Yarbrough|
Agency for Science, Technology and Research (A*STAR), Singapore