Removing `good cholesterol` receptor may help fight breast cancer
Washington: Eliminating a lipoprotein receptor known as SR-BI could reduce cancer cell and tumour growth, according to a new study.
In vitro and mouse studies revealed that depletion of the receptor resulted in a decrease in breast cancer cell growth.
SR-BI is a receptor for high-density lipoproteins (HDL) that are commonly referred to as ‘good cholesterol’ because they help transport cholesterol out of the arteries and back to the liver for excretion.
Previous lab research had revealed that mice fed a high cholesterol diet develop more advanced tumours and their tumours produce more SR-BI.
The research team, including Christiane Danilo, of the Department Stem Cell Biology and Regenerative Medicine at Thomas Jefferson University, and Philippe G Frank, PhD, an assistant professor in the Department of Stem Cell Biology and Regenerative Medicine at Jefferson, manipulated levels of SR-BI in human breast cancer cell lines and examined its effect on tumour formation in a mouse model.
In vitro, they found that ablation of the receptor protein in breast cancer cells led to a decrease in cancer cell proliferation, migration and invasion. Mouse models also showed that depletion of the receptor could confer protection against tumour growth.
Environmental factors, such as diet and obesity, have long been considered risk factors for the high breast cancer incidence in the Western world, and epidemiologic evidence indicates that cancer patients display abnormal levels of cholesterol carrying lipoproteins. However, the role of cholesterol in breast cancer had not yet been specifically examined.
“The results of this novel study show that depletion of SR-BI reduces cancer cell and tumour growth, suggesting that it could play an important role in breast cancer,” said Dr Frank.
“More studies are warranted to further characterize the role of SR-BI in tumour progression,” he added.
These findings were presented at the American Association for Cancer Research Annual Meeting 2012 by Jefferson’s Kimmel Cancer Centre researchers.
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