Breast cancer and diabetes could feed off each other with the cancer suppressing insulin and the diabetes feeding the tumour, a new study claims. Breast cancer is the most common form of cancer in UK women. One in seven will be diagnosed with it during their lifetime.
And 10 per cent of Brits over 40 have type 2 diabetes with the number of people living with the disease double what it was 15 years ago. However, past research has uncovered associations between the two diseases. Women with type 2 diabetes, for example, have a 20-27 percent increased risk of developing breast cancer.
Insulin resistance – a key characteristic of type 2 diabetes – has been linked with occurrences of breast cancer and poor survival Population studies suggest type 2 diabetes risk begins to increase two years after a breast cancer diagnosis and 10 years after, the risk is 20 percent higher in breast cancer survivors than in same-age women without the disease.
Up until now, these links have never been made out to be clear-cut or definitive, with some studies finding no associations at all. But new research published today in the journal Nature Cell Biology shows how breast cancer may suppress the production of insulin, resulting in type 2 diabetes, and the impairment of blood sugar control promotes tumour growth.
Study author Shizhen Emily Wang, pathology professor at UC San Diego said: “No disease is an island because no cell lives alone. In this study, we describe how breast cancer cells impair the function of pancreatic islets to make them produce less insulin than needed, leading to higher blood glucose levels in breast cancer patients compared to females without cancer.”
Dr Wang said the research was inspired by early work and guidance from Dr Jerrold Olefsky the associate dean for scientific affairs at UC San Diego. Dr Olefsky is the co-senior author of the study with Wang. According to these scientists, the problem is extracellular vesicles (EV), hollow spheres which are secreted or shed by cells that transport DNA, RNA, proteins, fats and other materials between other cells, like a sort of cellular postal system.
In this case, the cancer cells were found to be secreting micro-RNA-122 into the vesicles. Dr Wang said that when these vesicles reach the pancreas, they sometimes enter the islet cells responsible for insulin production and drop their miR-122 packages, which disrupts the islets’ important ability to maintain a normal glucose level.
She added: “Cancer cells have a sweet tooth. They use more glucose than healthy cells in order to fuel tumour growth and this has been the basis for PET scans in cancer detection. By increasing blood glucose that can be easily used by cancer cells, breast tumours make their own favourite food and, meanwhile, deprive this essential nutrient from normal cells.”
The research was done by using mice and found that slow-releasing insulin pellets or a glucose-lowering drug known as an SGLT2 inhibitor restored normal control of glucose in the presence of a breast tumour, which then suppressed the tumour’s growth. An inhibitor of miR-122, developed by Regulus Therapeutics in San Diego, is currently in clinical trials as a potential treatment for chronic hepatitis C.
It has been found to be effective in restoring normal insulin production and suppressing breast cancer tumour growth in mice. Dr Wang said: “These findings support a greater need for diabetes screening and prevention among breast cancer patients and survivors. These miR-122 inhibitors, which happen to be the first miRNA-based drugs to enter clinical trials, might have a new use in breast cancer therapy.”
