The Bcl-2 protein and the calcium pump
An unexpected discovery of how the body controls cell death has revealed a potential new therapeutic target.
A research team based at the School of Biosciences has already revealed the mechanism by which high alcohol intake can induce pancreatitis and its progression to pancreatic cancer. Now a new study, published in Current Biology, reveals a hitherto unknown interaction between two well known molecules, which has important implications for our understanding of inflammation and cancer in the pancreas as well as other organs.
The Cardiff team studied the protein Bcl-2, already known to be capable of inhibiting programmed cell death in all tissue types in the body. Cell death is vital to normal development, and under certain circumstances this protein can therefore promote tumour growth and cancer.
The Cardiff study of pancreas cells showed that removal of the Bcl-2 protein activated a molecule in the cell membrane which pumps calcium out of the cells. As the team expected, a lower level of Bcl-2 increased the level of programmed cell death. But they also found that the lack of Bcl-2 markedly protected against another much more dangerous form of cell death - necrosis, in which cells swell and burst, releasing their contents and causing severe inflammation. The team found the increased protection against necrosis was directly linked to increased activity of the calcium pump.
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