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Updated:05/30/2022 17:09h
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Breast cancer and type 2 diabetes appear to be distinctly different diseases, with only one thing in common. Breast cancer is the segunda neoplasia more diagnosed after some types of skin cancer; about 1 in 8 American women will develop invasive breast cancer in her lifetime. And diabetes is one of the biggest threats to global health.
However, previous research had found associations between the two diseases. Women with diabetes, for example, have a 20 to 27 percent increased risk of developing breast cancer. Insulin resistance – a key feature of diabetes – has been associated with breast cancer incidence and poor survival.
Population studies suggest that the risk of diabetes begins to increase two years after breast cancer diagnosis and that, at 10 years after diagnosis, the risk is 20% higher in breast cancer survivors than in women of the same age without breast cancer.
But these epidemiological links are not yet clear or definitive, and some studies have found no relationship.
In a new paper, in “Nature Cell Biology,” a research team led by scientists at the University of California San Diego School of Medicine describes a possible biological mechanism connecting the two diseases, in which breast cancer suppresses insulin production, which leads to diabetes, and impaired blood sugar control promote tumor growth.
“No disease is an island because no cell lives alone,” said study author Shizhen Emily Wang, of the UC San Diego School of Medicine. “In this study, we describe how breast cancer cells impair pancreatic islet function so that they produce less insulin than necessary, leading to higher blood glucose levels in breast cancer patients compared to women without cancer.
The culprits, according to Wang and Olefsky, are the extracellular vesicles (VE), hollow spheres secreted or shed by cells that transport DNA, RNA, proteins, fats, and other materials between cells, a kind of cargo communication system.
In this case, the cancer cells were found to secrete microRNA-122 in vesicles. Wang said that when the vesicles reach the pancreas, they can enter the islet cells responsible for insulin production, dispensing their cargo of miR-122 and damaging critical islet function in maintaining normal blood glucose.
“Cancer cells have a very sweet tooth,” says Wang. “They use more glucose than healthy cells to fuel tumor growth, and this has been the basis of PET scans for cancer detection. By increasing blood glucose they can use cancer cells easilybreast tumors manufacture their own favorite food and, meanwhile, deprive normal cells of this essential nutrient.”
The research was carried out using mouse models, in which slow-release insulin granules or a glucose-lowering drug known as an SGLT2 inhibitor were found to restore normal glucose control in the presence of a breast tumor , which in turn suppressed tumor growth.
“These findings support the need for increased screening and prevention of diabetes among breast cancer patients and survivors,” Wang said, noting that an inhibitor of miR-122, developed by Regulus Therapeutics Inc. in San Diego, is in currently undergoing clinical trials as a potential treatment for chronic hepatitis C, and has been found to be effective in restoring normal insulin production and suppressing tumor growth in mouse models of breast cancer.
“These inhibitorsand miR-122, which turn out to be the first drugs based on miRNA that enter clinical trials, could have a new use in breast cancer therapy,” adds Wang.
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