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Cancer cells have an extremely sweet tooth: they constantly need glucose – at much higher levels than normal cells – to get enough energy to multiply without restraint. This is why some cancers have been linked to type 2 diabetesthat is, with the inability to regulate blood glucose levels.
However, until now the mechanism that closely links diabetes and cancer was unknown. A new study published in Nature Cell Biology offers the first explanation for this relationship and ventures a new clinical pathway to combat the growth of breast cancer.
The link has been suspected for some time. Patients diagnosed with pancreatic cancer already had high blood sugar levels three years earlier, and those with higher sugar levels had larger tumor size.
Colon and breast cancers also seem closely linked to endocrine pathology. In addition, it had already been shown how the use of metformin, the main drug for type 2 diabetes, reduced the risk of cancer incidence and mortality.
The current study has focused on breast cancer. Women with diabetes have up to a 27% higher risk of developing it than those without. Secondly, already two years before the diagnosis of the tumor the risk of diabetes increaseswhich is maintained during the following decade: it is 20% higher than in women of the same age without breast cancer.
communication between cells
Researchers from the San Diego School of Medicine, University of California, have described a mechanism that can connect both diseases and that points to extracellular vesicles as the main culprit.
These elements are responsible for communication between cells. They are simply a container made of lipids that transport molecules from one place to another: proteins, other lipids, nucleic acids and even organelles of the cells themselves.
Shizhen Emily Wang, a professor at San Diego School of Medicine and leader of the study team, describes cancer cells as “greedy.” Increasing blood glucose allows them to eat more “while depriving normal cells of essential nutrients.”
Cancer cells would use extracellular vesicles to transport miR-122, a micro RNA (a non-coding RNA molecule used to regulate gene expression), to the pancreas, where it would enter the islets of Langerhans to alter their function of maintain proper glucose level.
The research has been done on mice. Those who showed high levels of miR-122 or who had a breast tumor were unable to secrete insulin and produced a high amount of glucose. By inhibiting the secretion of microRNA, it was possible to stop tumor growth.
MiR-122 levels were associated with glucose and lack of insulin. Therefore, the authors conclude that glycemic impairment caused by extracellular vesicles may control tumor progression and the incidence of type 2 diabetes in some breast cancer patients.
In this regard, a drug that inhibits miR-122 is already being studied in people as a potential treatment for hepatitis C, since this micro RNA is known to contribute to efficient replication of the virus.
So far, this drug has been shown to be effective in restoring insulin production levels and suppressing breast cancer tumor growth in mouse models. The next step will be to demonstrate its potential in humans.
“Well formulated hypothesis”
the oncologist Juan de la Habaspecializing in breast cancer, considers the study “a very well thought out hypothesis”, which delves into a previous line of research but goes a step further by suggesting the mechanism that links both diseases.
“This is good news for identification of a different mechanism linking breast cancer and diabetesDe la Haba explains that, despite the promise of metformin (“a well-known, widely used and safe oral antidiabetic”) and its good results in cell lines, its translation into humans did not generate conclusive answers.
Now, the approach of a microRNA that can influence tumor growth “is a novel hypothesis” that will have to be tested, in addition to breast cancer, in others such as colorectal or prostate cancer.
The also member of the Spanish Society of Medical Oncology points out that the Attempts have also been made to study the effect of glucose control in cancer, “but the studies have been methodologically improvable“.
The idea is that if some people with diabetes can see remission of their disease by following a very strict diet, it could also serve to prevent the consumption of glucose by tumor cells.
Thus, research has been carried out on intermittent fasting and other diets, although the results are confusing. However, De la Haba is optimistic: “There is a line of work with scientific activity, but it has yet to be defined.”
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