The research, reported in the journal Molecular Cell, identifies the protein beta-catenin as a key trigger in the development of cancer.
Researchers from the University of Utah, Salt Lake City, USA, showed that the p53 gene works via APC to reduce levels of beta-catenin. Since beta-catenin is responsible for cell growth cycles, this prevented the growth of tumors.
The researchers said the discovery of the mechanism represented a potential new target for therapeutic drugs.
|p53 works via APC to reduce levels of beta-catenin.
Researcher Dr Lori Matsumani said APC was known to regulate beta-catenin through a pathway that did not involve p53.
Dr Matsumani said, "Many changes happen when normal cells turn into malignancy. We need to explore and characterize the fundamental changes that define the critical stages of cancer development.
"We hypothesized that APC might provide a new link between p53 and cell-cycle regulation through degradation of beta-catenin."
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