Cells need to change their metabolism depending on their fuel supply. This means that when there is plenty of fuel in the form of food and oxygen, cells have plenty of energy to “spend” on growing and building new proteins. In cancer, cell metabolism is often altered, as cancer cells grow and divide at a much quicker rate than normal cells.
However, when food is scarce, cells need to save energy by shutting down their growth and recycling any old proteins that they don’t need anymore. This process is called autophagy.
Cell growth is controlled by a protein call mTOR, and autophagy is controlled by the protein AMPK, although both these pathways are very complicated and understanding of the details of these pathways is continuously developing a number of studies have shown that Folliculin interacts with both of these proteins, and is somehow involved in controlling the switch between cell growth and autophagy.
There is sometimes conflicting evidence as to the role Folliculin plays in affecting cell growth and autophagy. This is not uncommon in scientific research as the models used in laboratories can be very different from each other, and often only a single type of cell is studied at one time. This is therefore not always an exact representation of what would be occurring within a complex system e.g. a whole lung or kidney with many different cell types, however studying multiple cell types like this is very difficult in a laboratory setting.
When there is conflicting evidence in the scientific literature it is often representative of a very complicated situation where it is possible for the same protein to play opposite roles in the context of e.g. different cell types or stages of tumour development, and further research is needed to gain a better understanding of the protein.
Publication date: December 2014
Review date: June 2021