Targeting Aerobic Glycolysis Cancer at the Level of Phosphofructo-1-kinase

Aerobic glycolysis is a hallmark of proliferating cells; in cancer cells, it is the predominant metabolic profile, providing tumors benefits for growth and metastasis. The allosteric enzyme phosphofructokinase-1 (PFK-1) catalyzes the rate-limiting step of glycolysis. In tumor cells, the liver (L) isoform of this enzyme is predominantly expressed over the other isoforms at both the mRNA and protein levels. Our lab seeks to inhibit the PFKL enzyme in order to arrest glycolytic flux, which may reduce growth and survival of tumor cells. It has been shown that plasmids containing short hairpin (sh)RNA constructs that bind to PFKL mRNA have reduced the expression of the PFKL protein. This tool can be used to study the effect of PFKL knockdown and determine the value of designing a specific PFKL protein inhibitor. Note: Abstract extracted from PDF text