A recent study from the Institute for Cancer Research and CAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Biology, School of Life Science, University of Science and Technology of China, Hefei 230027, China shows that “Lin28/let-7 axis regulates aerobic glycolysis and cancer progression via PDK1.” This study was published in the 10 October issue of 2014 Nature Communications by Prof Zhang, Ma, and others.
On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Physiological and Pathological mechanisms that control glycolysis: SNAI inhibits glycolysis and cancer progression via down regulation of PDK1.
Idea Proposed/Formulated by: Dr L Boominathan Ph.D.
Citation: Boominathan, Physiological and Pathological mechanisms that control glycolysis: SNAI inhibits glycolysis and cancer progression via down regulation of PDK1, 21/October/2014, 07.03 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org
Significance: This study suggests that EMT protein SNAI, by increasing the expression of its target gene, it may increase the expression of PDK1. Thereby, it may enhance aerobic glycolysis, or warburg effect, in cancer cells. Thus, pharmacological formulations encompassing “SNAI inhibitors“ may be used to stall the progression of Cancer.
Amount: $300
Undisclosed information: How SNAI increases the expression of PDK1.
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