Researchers identify an oncogene regulated by nutrients.
Scientists from the Spanish National Cancer Research Center (CNIO) have discovered that the MCRS1 protein, in response to an excess of nutrients, induces an increase in the activity of mTOR (a mammalian/mechanistic target of Rapamycin); a protein that is altered in human diseases such as cancer and diabetes, processes associated with aging, as well as in certain cardiovascular and neurodegenerative pathologies. The team state that the data findings open up new possibilities for the development of drugs that block MCRS1 to treat cancer and diabetes. The opensource study is published in the journal Developmental Cell.
The team explain that under normal conditions, mTOR regulates essential cellular functions, such as protein synthesis and cell growth and proliferation. However, an overactive stimulation of mTOR in response to nutrients and growth factors, metabolic processes that are crucial in tumour biology, leads to an increase in cell growth and proliferation.
The researchers have now discovered how the MCRS1 protein, a protein associated with gene regulation and cell death processes, is capable of activating mTOR, and thus, stimulate cell proliferation. In this way, in human colorectal cancer samples, a correlation was found between increased MCRS1 activity and tumours with a high proliferation rate, as well as with a worse prognosis of the disease. The team would like it to be noted that although the current study published results obtained from colorectal samples, they are also studying the relationship between this protein and diseases of the liver, the primary metabolic organ.
The incidence of cancer and other related diseases has increased considerably in Western societies; this is partly due to an increased caloric intake and a more sedentary lifestyle. Therefore, unravelling the cellular processes that act in response to an excess of nutrients can contribute to achieve a better understanding of the biology of cancer and, consequently, is key to the fight against this disease, state the researchers.
The team plan to continue studying this gene using different genetically modified mouse models, where they can study what occurs when there is a gain- or loss-of-function. The team state they are already obtaining interesting results, but further research is necessary.