
USP7 facilitates brain tumor survival upon glucose deprivation by regulating phosphofructokinase muscle-type nuclear translocation in mice
We discover a novel function of PFKM in promoting glioma cell survival under glucose deficiency by switching metabolism from glycolysis to FAO. Upon GD, the levels of F-2,6-BP are decreased, leading to the enhanced interaction between USP7 and PFKM. USP7 then deubiquitinates PFKM K615 and promotes its nuclear translocation. Nuclear PFKM enhances c-Myc-dependent expression of CPT1B and the activity of FAO, and promotes tumor cell survival under GD.


