SYDNEY, Australia - Researchers at the University of Queensland uncovered a connection between a protein known to be a crucial controller of cell replication and cancer formation, and the way cells handle cholesterol.
The link found by the researchers, led by Rob Parton and John Hancock, was featured in a recent issue of the journal Nature Cell Biology. Parton said the research improved knowledge of "some of the factors that might lead to cells growing out of control in cancer," and showed cholesterol plays an unexpected role in cell organization.
Ras proteins help control cell replication and are known to be involved in certain types of cancer - the researchers say that Ras mutations occur in 90 percent of pancreatic cancers, 50 percent of colon cancers and 30 percent of acute leukemias.
The work by Parton, of the Centre for Microscopy and Microanalysis, and Hancock, in the Queensland Cancer Fund Laboratory of Experimental Oncology, Department of Pathology, initially involved mutating another type of protein, called caveolin proteins.
Those proteins earlier had been shown to stop cells being infected by certain viruses that normally cause tumors.
Parton said the mutated caveolin proteins stopped the Ras protein, but later work showed it did so by affecting the way the cells handled cholesterol.
He said the findings suggested that Ras proteins must associate with certain, cholesterol-rich areas of the membrane in order to control cell replication. The findings also suggest that a major function of caveolins was to control how cholesterol is transported around the cell and delivered to areas containing Ras proteins.