In the human body, mTOR (“mechanistic target of rapamycin”) is a biochemical process for instructing a cell to grow and divide in response to an appropriate level of nutrients. When the mTOR pathway is reduced a cell moves into a second mode. Here the cell does not grow, but instead recycles old proteins and cleans itself up inside of unwanted matter. A common term for this viable but non-active state is “senescence.”
This is a survival mode where cells remain idle. The remarkable thing about this physiological state is that it appears to delay aging. However, at the same time it may also contribute to the malignancy of cancer.
How mTOR performs this function has never been cleat to scientists, until now. Scientists based at the U.K. Medical Research Council Clinical Sciences Centre (CSC), which is located at Imperial College, London have put forward an explanation has to how mTOR operates.
Research has shown how age-related diseases and cancer might be better controlled, through interfering with the mTOR function stopping cells from slowing down. This is because senescent cells are associated with tumours. This is for a couple of reasons. First, the immune system, as someone ages, becomes capable of flushing such cells out of the body. This, in turn, can contribute to the aging of our tissues, by making them less functional.
Secondly, cells in this state secrete proteins termed ‘Senescence Associated Secretory Phenotypes’. These proteins can promotes inflammation and, under certain conditions, in enhance the malignancy of tumors.
These effects were shown in studies where an mTOR inhibitor chemical called rapamycin was used. Studies were run in cell cultures and in mice. The rapamycin successfully blocked the formation of the proteins in high quantities. Rampamycin is produced by the bacterium Streptomyces hygroscopicus.
The conclusion is if: “blocking mTOR can suppress the harmful effects of senescent cells, then drugs that target mTOR or its mediators may improve our healthspan.”
The research has been published in the journal Nature Cell Biology. The paper is titled “mTOR regulates MAPKAPK2 translation to control the senescence-associated secretory phenotype.”
