Fig. 3: Disrupting VDAC2 in NSTCs potentiates the acquisition of GSC properties. | Cell Death & Disease

Fig. 3: Disrupting VDAC2 in NSTCs potentiates the acquisition of GSC properties.

From: VDAC2 interacts with PFKP to regulate glucose metabolism and phenotypic reprogramming of glioma stem cells

Fig. 3

a Western blot analyses of the GSC markers (CD133, SOX2, and OLIG2) and VDAC2 in NSTCs expressing shVDAC2 or shNT. The levels of GSC markers CD133, SOX2, and OLIG2 are increased in NSTCs expressing shVDAC2 compared with those expressing shNT. b In vitro limiting dilution analysis of the self-renewal capacity of NSTCs expressing shVDAC2 or shNT. Disruption of VDAC2 increases the self-renewal capacity of NSTCs. c, d Representative images of tumor cell clones (c) and quantification of clone formation efficiency (d) in NSTCs expressing shVDAC2 relative to those expressing shNT. Silencing VDAC2 expression promotes the clone formation ability of NSTCs (***p < 0.001). e, f Representative bioluminescent images (e) and the quantification (f) of xenografts derived from NSTCs expressing shVDAC2 or shNT at day 10 and day 20 after tumor cell implantation. Silencing of VDAC2 markedly promotes tumor formation of xenografts derived from NSTCs. p photons, sr steradian (***p < 0.001). g Kaplan–Meier survival analysis of mice bearing xenografts derived from NSTCs expressing shVDAC2 or shNT. Silencing of VDAC2 reduces the survival of tumor-bearing mice. n = 5/group. h, i Quantification of the level of VDAC2 (h) or GSC marker SOX2 (i) in GBM xenografts derived from NSTCs expressing shVDAC2 or shNT by IHC staining (***p < 0.001)

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