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Controlling `bad cholesterol` may prevent tumour growth
One of the key factors for this process are proteins we all have that, in larger quantities, may cause a decrease in the amount of LDL receptors to excrete the cholesterol.
Toronto: Controlling 'bad cholesterol' may help reduce the growth of cancer cells, say scientists who found that tumours may use lipids as "building blocks" to grow.
Scientists studied how tumour cells grow by scavenging very low-density lipoproteins (VLDL) and low-density lipoproteins (LDL), and what mechanisms can be used to reduce the malignant cells' growth.
Researchers from the University of Alberta in Canada and Medical University of Graz in Austria found that tumours not only use lipids to grow, but they can regulate their host's lipid metabolism to increase production of these lipids.
The "bad cholesterol" binds to LDL receptors in the liver, the organ in charge of degrading it and excreting it from the organism as bile.
"Cancer cells need lipids to grow. They can make their own lipids or get more from the host because these cells grow so fast," said Richard Lehner, from the University of Alberta.
"The tumour signals to the liver: 'I need more cholesterol for growth' and the liver is reprogrammed to secrete those lipids," Lehner said.
One of the key factors for this process are proteins we all have that, in larger quantities, may cause a decrease in the amount of LDL receptors to excrete the cholesterol.
The tumour affects these proteins to reduce clearance of cholesterol from the blood, leaving the LDL for cancer to feed off of it.
These findings led researchers to an interesting hypothesis: minimising the liver's production of LDL would deprive a tumour from its constant supply and therefore reduce its possibility of growth.
Their experiments in pre-clinical models proved to be successful, confirming lower tumour development with the regulation of the proteins that affect production of VLDL (precursors of LDL) and uptake of LDL by receptors from the liver.
The study was published in the journal Cell Reports.