We’ve been providing a fair bit of coverage on cancer recently, and today will be no exception.
Unfortunately, right now I can offer little more than a pointer to the research article (published in The Journal of Clinical Investigation). I’m still working my way through it and may not have the time to return. So if you’re interested in sharing your thoughts on it, please add to the comments below!
Increased sugar uptake promotes oncogenesis via EPAC/RAP1 and O-GlcNAc pathways.
The signaling mechanisms triggered by glucose metabolism have been widely investigated ina number of diseases, such as diabetes. There is also ample evidence — starting with Warburg’s findings(2) — that tumors require more aerobic glycolysis and more recently, that oncogenic pathways will increase glucose uptake and metabolism, interpreted as a necessary step for increased growth and increased energy production for tumors(6-8). The reverse (i.e., a direct causative role of increased glucose uptake and its relation to metabolic patterns) was originally reported in chick embryo fibroblasts and their RSV-transformed counterparts more than 3 decades ago, as discussed above. We believe ours is the first mechanistic study to shed light on how a breakdown in homeostasis of sugar uptake and its metabolic signalign could be instrumental in malignant progression.
Our findings provide a hitherto-undescribed direct role of increased aerobic glycolysis in inducing he cancer phenotype, in which increased glycolytic activity regulates the canonical oncogenic pathways dynamically and reciprocally. These results may provide additional evidence for how hyperglycemia in diseases such as obesity and diabetes could provide a microenvironment that results in higher risk of some cancers (69.70). Additionally, our findings may explain how small molecules, such as metformin (used for treatment of diabetes and known to lower blood glucose levels), decrease the risk and mortality of several types of cancers (69,71). (source)