Release date: 2012-11-29
Recently, an animal study conducted by researchers at the Lombardi Comprehensive Cancer Center at Georgetown University confirmed the increased activity of glucose-driven tumor growth-promoting genes.
In a study published in the journal Cell Cycle, scientists report that high blood sugar levels in cancer mice are associated with increased expression of the mutant p53 gene. Normal p53 is a tumor suppressor gene, but many scientists believe that as a proto-oncogene, mutant p53 promotes tumor growth. Mutant p53 expression levels are high in many types of tumors and have long been associated with cancer aggressiveness, resistance therapy, and relapse after treatment.
But the findings don't mean that cancer patients should cut sugar in their diet, a senior researcher in the study, Maria Laura Avantaggiati, MD. We have not studied the effects of glucose on the growth of human cancer cells, so we cannot make this conclusion at this point. In addition, there are many different types of p53 gene mutations in practice, and we have only studied some of them.
Avantaggiati added that the study tested different dietary diets and found that complete starvation did not have any effect on the level of mutant p53 in laboratory-cultured cancer cells. She also added that we also studied whether different components of the diet, in addition to glucose, would also contribute to the expression of tumor p53 mutations.
Exfoliation of glucose causes the cells to clear the mutant protein. In this study, the researchers sought to understand how the mutant p53 gene is degraded in tumor cells. This question is very important, Avantaggiati said, not only because most people contain too many mutant p53 proteins in their tumors, but researchers now believe that current chemotherapy drugs actually increase the mutation of p53 in cancer cells. The amount that leads to the resistance that these medications may encounter.
In cultured cells, the researchers studied the link between glucose exfoliation and autophagy. Autophagy is a process that removes damaged organelles from cells and misfolded proteins.
Mutant p53 proteins are misfolded, but they are usually not efficiently degraded. However, when glucose is exfoliated, autophagy is induced, a process that eliminates protein misfolding, which we hope to see, Avantaggiati said. However, this process also carries a problem, which is often shut down by the mutant p53. But now because these cancer cells contain very small p53 proteins, autophagy can degrade proteins and drive cancer cell death.
The researchers then conducted a series of studies to establish this connection in animal models. In a transgenic mouse model with mutant p53 protein, they found that after feeding a low-carbohydrate diet (hypoglycemia), the mice had a normal caloric load, and the amount of mutant p53 protein in their tissues was significantly reduced, while the high-carbohydrate diet The mouse is the opposite.
This suggests that mutant p53 protein levels are glucose sensitive, but more research is needed to determine if this phenomenon has an effect on tumor growth. To answer this question, scientists conducted experiments to test the growth of human lung cancer cells in low or high carbohydrate environments.
They found that tumor growth was prevented in mice fed a low-carbohydrate diet, but tumor-mutant p53 protein expression was degraded by autophagy. However, the artificial mutant p53 protein could not be eliminated, and the growth of cancer cells was continued without being affected by the glucose content in the diet. This suggests that degradation of the p53 gene mutation is part of the reason why a low-carbohydrate diet reduces tumor growth.
Source: Bio Valley
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