The past few years we have seen quite a bit of research on cancer and sugar; it has also been largely suggested that the two are grossly connected. Well, a new study says that sugar and cancer are, in fact, connected in at least one way.
It began in 2008, but this new study reveals that sugar has the power to “awaken” cancer cells and make tumors more aggressive. More specifically, the research team—which hails from the University of Leuven (KU Leuven), the University of Brussels (VUB), and the Vlaams Institute for Biotechnology (VIB)—says they were able to clarify something called “The Warburg effect.” This is a phenomenon in which cancer cells rapidly break down sugars to stimulate tumor growth.
Most importantly, though, the study provides distinctly positive evidence of a direct correlation between sugar and cancer.
Lead study author Johan Thevelein, PhD, notes: “Our research reveals how the hyperactive sugar consumption of cancerous cells leads to a vicious cycle of continued stimulation of cancer development and growth.” The KU Leuven professor goes on to say, “Thus, it is able to explain the correlation between the strength of the Warburg effect and tumor aggressiveness. This link between sugar and cancer has sweeping consequences. Our results provide a foundation for future research in this domain, which can now be performed with a much more precise and relevant focus.”
In addition, the study authors comments, “We now reveal an evolutionarily conserved mechanism linking fermentation to activation of Ras, a major regulator of cell proliferation in yeast and mammalian cells, and prime proto-oncogene product.”
In this study, they note that a yeast mutant with an overactive glucose to glycolysis influx and a hyperaccumulation of Fru1,6bisP, indicates there is hyperactivation of the Ras. This, they say, “causes its glucose growth defect by triggering apoptosis. Fru1,6bisP is a potent activator of Ras in permeabilized yeast cells, likely acting through Cdc25. As in yeast, glucose triggers activation of Ras and its downstream targets MEK and ERK in mammalian cells. Biolayer interferometry measurements show that physiological concentrations of Fru1,6bisP stimulate dissociation of the pure Sos1/H-Ras complex. Thermal shift assay confirms direct binding to Sos1, the mammalian ortholog of Cdc25.”
In conclusion Dr. Thevelein notes that “the main advantage of using yeast was that our research was not affected by the additional regulatory mechanisms of mammalian cells, which conceal crucial underlying processes. We were thus able to target this process in yeast cells and confirm its presence in mammalian cells. However, the findings are not sufficient to identify the primary cause of the Warburg effect. Further research is needed to find out whether this primary cause is also conserved in yeast cells.”