CANCER can be prevented by ‘molecular scissors’, a protein that is vital for repairing damaged and abnormal DNA, researchers have stated in a discovery that could pave the way for new treatments of the disease in the future.
Scientists from the University of Dundee (UoD), Dundee, UK found that the protein, FAN1, is extremely effective at impeding the development of cancer, and may become a molecular target for treatment.
The role of the structure-specific nuclease, FAN1, was first discovered in 2010 when Prof John Rouse, Programme Leader in Protein Phosphorylation, UoD, highlighted its importance in repairing DNA. The study showed that the FAN1 protein is specifically recruited to areas of DNA damage and buffers genome instability.
Now, under the direction of Prof Rouse, Dr Christophe Lachaud, Postdoctoral Researcher, UoD, and his colleagues, have discovered that FAN1 also plays an important role during the chromosome replication that occurs in cell division. Specifically, the recognition and cutting of particular types of abnormal structures within the cell. At the same time, this finding suggests that some cancers may be caused by failure of FAN1 to cut DNA correctly.
Prof Rouse explained: “We showed that FAN1 can recognise these [sic] dangerous structures, and uses its cutting activity to make them less toxic. We found that when we switch off the ability of FAN1 to cut these structures the genome starts to become abnormal and breaks apart, which means the instruction manual has become corrupted.”
“Other scientists have shown that FAN1 is mutated in pancreatic cancers, and we showed that in these cancers FAN1 is not able to recognise the abnormal structures that need to be cut. This leads the genome of these cells to become abnormal, accounting for the cancers.”
The implications are especially strong for cancers of the lung, liver, and pancreas, though it is thought that this finding may lead to the development of new treatments for a variety of cancers. The research is ongoing as the team attempts to find a drug that is selectively toxic to cells that contain mutated or defective FAN1.