A Study On The SIRT1 On Colorectal Cancer Cell Glycolysis By Deacetylating PKM2

It was demonstrated that cancer cells produce ATP depending on glycolysis even in the existence of sufficient oxygen supply,a phenomenon named Warburg effect or aerobic glycolysis.SIRT1 is a member of the sirtuin family.Nicotinamide adenine dinucleotide(NAD~+)is required for SIRT1 to deacetylate lysine residues on target proteins.It was expressed aberrantly in different kinds of cancer.The role of SIRT1 in tumor glycolysis function has not been well demonstrated.In this study,the overexpression of SIRT1 inhibits colon cancer cell glycolysis and suppresses proliferation.Particularly,SIRT1 was down regulated in colorectal cancer compared with the normal tissue.Over expression of SIRT1inhibits cancer cell to uptake glucose and produce lactate.It could bind with PKM2 and deacetylate PKM2 at K433 residue.PKM2 was export to the cytoplasm from nuclear and acquired an increased activity.The anabolism was decelerated by reduced accumulation of mabolism intermediates.As a result,the proliferation of colorectal cancer was suppressed.