Discovery of a mechanism that turns tumour cells into sugar ʻaddictsʼ

On the left, healthy cells with glucose receptors (in red). On the right, tumor cells with glucose receptors (in red).
On the left, healthy cells with glucose receptors (in red). On the right, tumor cells with glucose receptors (in red).
Research
(11/04/2014)

Nearly a hundred years ago, research demonstrated that cancer cells feel a special appetite for a type of sugar called glucose. Tumour use glucose like a sports car uses gasoline: it depends on it to burn faster, to grow and to multiply rapidly. It is not an energy-efficient process, but it super-accelerates cell division in what is known as the Warburg effect, which was described in 1927.

On the left, healthy cells with glucose receptors (in red). On the right, tumor cells with glucose receptors (in red).
On the left, healthy cells with glucose receptors (in red). On the right, tumor cells with glucose receptors (in red).
Research
11/04/2014

Nearly a hundred years ago, research demonstrated that cancer cells feel a special appetite for a type of sugar called glucose. Tumour use glucose like a sports car uses gasoline: it depends on it to burn faster, to grow and to multiply rapidly. It is not an energy-efficient process, but it super-accelerates cell division in what is known as the Warburg effect, which was described in 1927.

To date, little was known about how healthy cells go from balanced energy consumption to this calorific ʻfast foodʼ need in the tumour cell. An article published in Nature Communications led by Manel Esteller, professor of Genetics at the Faculty of Medicine of the University of Barcelona (UB) and ICREA research professor at the Bellvitge Biomedical Research Institute (IDIBELL), where he directs the Epigenetics and Cancer Biology Programme, provides an important clue to understand this process. The study shows that in one out of four human tumours, there is an excess of glucose receptors in the external face of the cell membrane and this protein acts as a magnet attracting all the glucose from the bloodstream.

Esteller explains how it was found: “We were looking for genes that did not work well in tumour cells and we found an altered one, but we did not know what its function was. Then, we discovered that it was responsible for removing excess glucose receptors”. This enabled to identify the problem: the gene that should degrade glucose receptor is inactivated in healthy conditions. “In tumour cells, the receptor is over-activated; it captures all glucose molecules around it and uses them to obtain quick energy to proliferate”, points out Esteller. “It is a cancer that has become addicted to this calorific molecule”, he concludes.

“The interesting thing is to study whether future treatments, based on drugs which fight against a tumour and, besides, quit the energy source, achieve tumour death as tumour cells are not easily adapted to use other substrates to obtain energy to survive”, highlights Esteller.

 

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