1100 GMT February 22, 2020
The team discovered that a specific protein (PCL1) kicks a famous cancer-associated protein (p53) into action in our bodies. The p53 protein suspends cells in a dormant, non-dividing state called 'quiescence'. When cells are in this state, they are much harder to target therapeutically, Medical Xpress reported.
As a result, the scientists hope that blocking PCL1 will set a chain of events in motion that will cause cancer cells to leave the cover of quiescence so that they can be targeted and eliminated.
Assistant Professor in Medical Molecular Genetics at Trinity, Dr. Adrian Bracken, led the team, said, "Often, treating a cancer patient with chemotherapy or radiation doesn't work out as planned. The tumor shrinks at first, but the cancer stem cells within can survive and eventually seed the growth of new, more aggressive cancers. When cancer stem cells are in this state of cellular quiescence, the treatments can really only be partially effective."
Therefore, a key challenge in medicine has been to develop a means to target cancer stem cells and knock them out of their dormant, quiescent state, so they can then be killed by standard cancer therapies.
The team's research encompasses multiple disciplines including cancer cell biology, computer-predictive chemistry and evolutionary genetics.
The study's lead author, Dr. Gerard Brien, demonstrated that PCL1 binds to — and boosts — the function of the p53 protein, and that this is required for p53 to activate cellular quiescence.
Bracken added: "Our discovery that PCL1 has acquired a new function during the relatively recent evolution of mammals was very interesting, while the realization that it teams up with the famous p53 protein represented an important breakthrough in the field of cancer biology."
"We are now excited about using this new knowledge to develop a strategy to target cancer stem cells by knocking them out of their dormant state, thereby making them more amenable to standard chemotherapy and radiotherapy."