Skip to main content
. 2018 Sep 24;9(10):988. doi: 10.1038/s41419-018-1015-x

Fig. 5. PFK inhibitor compromises the effect of VDAC2 disruption on glycolytic reprogramming and GSC phenotypic transition.

Fig. 5

a Analysis of PFK activity in shVDAC2-expressing NSTCs treated with or without PFK inhibitor CTZ. CTZ treatment impairs the effect of VDAC2 silencing on the promotion of PFK activity (**p < 0.01). b Analysis of lactate production in shVDAC2-expressing NSTCs treated with or without PFK inhibitor CTZ (**p < 0.01). c Western blot analyses of the GSC markers CD133, SOX2, and OLIG2 in shVDAC2-expressing NSTCs treated with or without PFK inhibitor CTZ. d In vitro limiting dilution assay of shVDAC2-expressing NSTCs treated with or without PFK inhibitor CTZ. Inhibition of PFKP by CTZ effectively compromises the VDAC2 disruption-induced self-renewal of NSTCs. e Quantification of clone formation efficiency of shVDAC2-expressing NSTCs treated with or without PFK inhibitor CTZ (***p < 0.001)