Fig. 6
From: KPNA2 promotes metabolic reprogramming in glioblastomas by regulation of c-myc
Subcellular redistribution of E2F1 caused by knockdown of KPNA2 contributed to the deregulation of c-myc. The subcellular distribution of E2F1 in the KPNA2-shRNA and control transfected cells by nuclear/cytosol fractionation (a) and immunofluorescence (b) was shown. Error bars indicated the mean ± s.d. of three independent views. MEK1/2 was used as the cytoplasmic control and Histone H3 as the nuclear control. *P < 0.05, **P < 0.01. c Co-immunoprecipitation analysis was presented between KPNA2 and E2F1 in the U87 cells. d Expressions of c-myc were analyzed by immunoblotting in the KPNA2-overexpressed U87 cells silenced with E2F1 or not. e The KPNA2-overexpressed U87 and U251 cells were transfected with pGL2-c-myc, a vector encoding E2F1-shRNA or its comparative control, and pSV-Kerilla. Values in graphs represented the mean of Fluc:Rluc activity±s.d. performed in triplicate. **P < 0.01