Scientists at Jefferson Medical College and the Kimmel Cancer Center at Thomas Jefferson University in Philadelphia have found how a gene can dim the power production in the cell and in turn scale up its cancer-producing activities.
Two new studies provide stunning evidence suggesting that cyclin D1 which is found in up to eight times normal amounts in half of all breast cancers can cause a shift in the cancer cell's metabolism, changing its focus from energy production to proliferation. The findings, they say, may point to new therapeutic strategies against cancer.
Reporting last month in the journal Molecular and Cellular Biology, Kimmel Cancer Center director Richard G. Pestell, M.D., Ph.D., Professor and Chair of the Department of Cancer Biology at Jefferson Medical College, and colleagues showed for the first time that cyclin D1 normally involved in promoting cell division inhibits the size and activity of the cell's energy-making mitochondria.
In a separate report in August in the Proceedings of the National Academy of Sciences (PNAS), Dr. Pestell and a different team identified the mechanism behind cyclin D1's mitochondrial takeover. The research, taken together, shows that the inhibition leads to increased proliferation of cancer cells.
"From the cancer cell's point of view, the inhibition allows the cell to shift its biosynthetic priorities it allows it to shift from making mitochondria themselves to synthesizing DNA and making the cell proliferate," says Dr. Pestell.
"Cyclin D1 shifts the individual cell's metabolism away from making mitochondria and towards cellular proliferation and the various genes involved in promoting such proliferation," he says.
The mitochondria often are called the "powerhouse" of the cell because they produce about 90 percent of the body's energy. They are located in the cytoplasm outside of each cell's nucleus.