Cancer cells are extremely sweet: they need glucose continuously - at much higher levels than normal cells - to get enough energy that makes them multiply without brake.That is why some cancers with type 2 diabetes have been related, that is, with the inability to regulate blood glucose levels.
However, so far the mechanism that closely relates diabetes and cancer was unknown.A new study published in Nature Cell Biology offers the first explanation to this relationship and adventure a new clinical route to combat breast cancer growth.
The link was already suspected for a long time.Patients diagnosed with pancreatic cancer already had high blood sugar levels for three years before, and those with higher sugar levels had a larger tumor size.
Colon and breast cancers also seem closely linked to endocrine pathology.In addition, it had already proven how the use of metformin, the main medication for type 2 diabetes, reduced the risk of incidence and mortality from cancer.
The current study has focused on breast cancer.Women with diabetes have a risk of up to 27% greater than those who do not.On the other hand, two years before the diagnosis of the tumor, the risk of diabetes grows, which is maintained during the next decade: it is 20% higher than in women of the same age without breast cancer.
communication between cells
Researchers at the San Diego School of Medicine, from the University of California, have described a mechanism that can connect both diseases and that points to extracellular vesicles as the main responsible.
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 lipistic, nucleic acids and even organelles of the cells themselves.
Shizhen Emily Wang, professor at the San Diego School of Medicine and team leader who conducted the study, describes cancer cells as "sweet tooth."Increasing blood glucose allows them to feed more "and, while, they deprive normal cells of essential nutrients."
Cancer cells would use extracellular vesicles to transport MIR-122, a micro RNA (a non-coding RNA molecule that serves to regulate the expression of the genes), to the pancreas, where it would enter the Langerhans islets to alter its function ofMaintain the proper level of glucose.
The investigation has been carried out in mice.Those who showed high levels of MIR-122 or who had a breast tumor were not able to secrete insulin and production a high amount of glucose.By inhibiting the secretion of the micro RNA, it was possible to stop tumor growth.
MIR-122 levels were associated with glucose and lack of insulin.Therefore, the authors conclude that the glycemic deterioration caused by extracellular vesicles can control the progression of the tumor and the incidence of type 2 diabetes in some patients with breast cancer.
In this regard, a medicine that inhibits MIR-122 as a potential treatment for hepatitis C is already being studied in people, since it is known that this micro RNA contributes to an efficient replication of the virus.
So far, this drug has been effective restoring insulin production levels and suppressing tumor growth of breast cancer in mice models.The next step will be to demonstrate its potential in humans.
"well raised hypothesis"
The oncologist Juan de la Haba, specialized in breast cancer, considers the study "aVery well raised hypothesis ", which delves into a line of previous research but that takes another step by suggesting the mechanism that relates both diseases.
"It is good news for the identification of a different mechanism that links breast cancer and diabetes."Haba explains that, despite the promising of metformin ("an oral antidiabetic, very used and safe") and its good results in cell lines, its translation to humans did not generate conclusive answers.
Now, the approach of a microarn that can influence tumor growth "is a novel hypothesis" that will have to be verified, in addition to breast cancer, in others such as colorectal or prostate.
The vowel of the Spanish Society of Medical Oncology points out that the effect of glucose control has also tried to study in cancer, "but the works have been methodologically improvable."
The idea is that, if some people with diabetes can see the remission of their disease by wearing a very strict diet, it could also serve to avoid glucose consumption by tumor cells.
Thus, research on intermittent fasting and other diets have been carried out, although its results are confused.However, Haba is optimistic: "There is a line of work with scientific activity, but it still needs to be defined."
