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November 1, 2017 | 2 minute read

Sugar-Cancer Mechanism Link Identified in Cell Study

A study in yeast cells provides new clues to understand why cancer cells metabolize glucose without oxygen, a long recognized phenomenon called the Warburg effect. The paper was published in Nature Communications.

Most human cells use glucose as their primary energy source and most healthy body cells use oxygen to break down that sugar molecule into usable energy. Both humans and yeast can use an alternative  albeit less efficient – method for turning sugar into useable energy but usually only when oxygen is not available. In the 1920s, Otto Warburg saw that cancer cells use this process to break down sugar, even when oxygen is plentiful.

In this study, the scientists examined the control of genes in response to the metabolic products of sugar metabolism. They showed that one metabolite (fructose-1,6-bisphosphate, or Fru1,6bisP for short), activated the Ras gene. The Ras gene is one of the most commonly mutated in human cancers, leading to unchecked cell proliferation and survival. This process appears to be evolutionary conserved in yeast and cancer cells, the authors conclude.

More experiments found that the concentration of this metabolite and Ras proteins do not appear to directly correlate with cell proliferation rates, regardless of glucose levels. This suggests additional mechanisms regulate cell proliferation.

Glucose is the basic form of sugar. Table sugar, the sugar commonly used in foods, is a mixture of both glucose and sucrose. AICR research shows that sugar by itself is not a cause of cancer. Sugar can indirectly lead to increased cancer risk if excess consumption of sugar foods leads to being overweight. Overweight and obesity is a cause of 11 common cancers.

Here’s AICR recommendations on sugar.

The study was supported by the Agency for Innovation by Science and Technology, the Research Fund, the Fund for Scientific Research—Flanders, Interuniversity Attraction Poles Network P6/14 and P7/40, and the Research Fund of the KU Leuven and the Belgian Foundation Against Cancer.

Source: Ken Peeters, Frederik Van Leemputte, Baptiste Fischer, Beatriz M. Bonini, Hector Quezada, Maksym Tsytlonok, Dorien Haesen, Ward Vanthienen, Nuno Bernardes, Carmen Bravo Gonzalez-Blas, Veerle Janssens, Peter Tompa, Wim Versées, Johan M. Thevelein. Fructose-1,6-bisphosphate couples glycolytic flux to activation of Ras. Nature Communications, 2017; 8 (1) DOI: 10.1038/s41467-017-01019-z

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