Researchers from Singapore and Great Britain have discovered, after several studies, a mechanism that explains why the appearance of cancer is associated with an unhealthy diet or with uncontrolled metabolic diseases.
According to LONGEVITY Magazine, the scientists involved in this research used mouse models, human tissue and human breast organoids grown in the laboratory. The results showed that changes in glucose metabolism could favor the development of cancer by temporarily disabling a gene that protects us from tumors, called BRCA2, notes Science Alert.
“These findings raise awareness of the impact of diet and weight control in managing cancer risk,” says first author of the new study, pharmacologist oncologist Li Ren Kong from the Institute of Cancer Sciences in Singapore.
Recent studies have found that a mutation in one of the two BRCA2 genes of a cell is involved in the development of various types of cancer. Interestingly, mouse and human cells with this mutation do not show the usual signs of genetic instability seen in cells with both copies of the mutant gene.
In mice, only one copy of BRCA2 has been found to be affected, but it does not appear to cause major problems in organ development or DNA repair in most tissues. However, cells that have this mutation are more vulnerable to stress, such as exposure to environmental toxins, which ultimately cause functional problems, the study reveals.
Results among people
The research team first examined people who inherited a defective copy of the BRCA2 gene. They found that these people’s cells were more sensitive to methylglyoxal (MGO), which is produced when cells break down glucose for energy.
In conditions such as diabetes, where MGO levels are high due to high blood sugar, these harmful compounds contribute to the complications of the disease.
The researchers found that MGO can temporarily disable the tumor-suppressing functions of the BRCA2 protein, leading to mutations linked to cancer development. This effect could be observed in non-cancerous cells, as well as in tissue samples from patients, in some cases of human breast cancer and in mouse models of pancreatic cancer.
Overall, this suggests that changes in glucose metabolism may disrupt BRCA2 function via MGO, contributing to cancer development and progression.
However, high levels of MGO can be regulated by means of appropriate medication, but also by adopting a healthy diet. “High levels of methylglyoxal can usually be controlled with medication and a good diet, creating avenues for proactive measures against cancer initiation.”
According to the researchers, these results could lead to cancer prevention or early detection strategies.
The research was carried out on a small sample of human tissue, and the results were published in the journal Cell.
