RESEARCH PROJECTS
Cancer cells are known to consume higher amounts of glucose (Warburg effect or aerobic glycolysis) associated with upregulated expression of genes involved in glucose metabolism. In our experimental work with glucose metabolism, we identified a previously undescribed subpopulation that is able to survive in the absence of glucose supply. We found that these subpopulation cells were those who were able to almost completely shift their metabolism from glycolysis to oxidative phosphorylation, resuming their proliferation following an adaptation period of 3-4 weeks. The metabolic shift toward enhanced oxidative phosphorylation is accompanied by production of increased reactive oxygen species (ROS) which leads to DNA damage resulting in disturbances in chromatin organization.
The ketogenic diet (KD) based on high fat (over 70% of daily calories), low carbohydrate, and adequate protein intake, has become popular due to its potential therapeutic benefits for several diseases including cancer. Under KD and starvation conditions, the lack of carbohydrates promotes the liver to produce ketone bodies (KB) from fats as an alternative source of metabolic energy. KD and starvation may affect the metabolism in cancer cells, affecting tumor properties. Due to controversial results of ketone bodies on cancer cell growth, survival, and progression we hypothesized that effect of KB may affect cancer cells in two different ways, simultaneously.
Viral infection leads to inflammatory processes to combat the disease. Interferons (IFN) are kind of “first responder” molecules which among other functions are responsible for initiation of massive cytokine production to report the immune system about viral invasion. At the same time, unrestrained immune response may be accompanied by overexcited increase of pro-inflammatory cytokines synthesis leading to a phenomenon called the “cytokine storm”. Therefore, modulating the inflammatory response is an important strategy for treating consequences of viral infection.
