20 April 2012
If you have ever experienced the frustration of a power outage you can appreciate how much we rely on energy to survive. The same is true for cancer cells - only in this case Prof Mike Berridge and his team are happy to be the ones pulling the plug.
It has long been known that cancer cells use nutrients differently than normal cells to produce energy. Elevated glucose uptake for example is a common property of metastatic tumours (cancers that spread). It is this increased need for glucose that makes cancer cells stand out from normal cells on positron emission tomography (PET) scans of tumours.
High glucose uptake is associated with glycolytic metabolism, a term used to describe cells that derive their energy from a pathway that does not involve burning oxygen via mitochondria - the more efficient aerobic energy powerhouses of the cell. Switching to a predominantly glycolytic metabolism has been suggested as a key survival strategy of cancer cells.
To investigate how energy metabolism affects the ability of cancer cells to form tumours and spread, Research Fellow An Tan developed glycolytic models of melanoma and breast cancer cells. The mitochondria in these cells are not able to produce energy, so the cells rely entirely on glycolysis for their survival.
Based on previous findings it was anticipated that these glycolytic cells would be highly cancerous, however An instead found that the cells were unable to metastasise and form tumours in the lungs. Even more surprising, the tumours that did form appeared to have somehow acquired an ability to reactivate their energy-producing mitochondria.
Subsequent analysis of the cells by An and Dr James Baty has revealed a startling new phenomenon in tumour biology. The outcome has therapeutic implications for controlling the growth and metastasis of glycolytic tumours.