Figure 5: DAXX disruption inhibits intracranial tumour growth and improves survival rate in PTEN-deficient GBM-PDX models. | Nature Communications

Figure 5: DAXX disruption inhibits intracranial tumour growth and improves survival rate in PTEN-deficient GBM-PDX models.

From: PTEN regulates glioblastoma oncogenesis through chromatin-associated complexes of DAXX and histone H3.3

Figure 5

(a,b) Representative fluorescence molecular tomography (FMT) images of mice intracranially engrafted with PTEN-deficient (a) or PTEN-expressing (b) GBM-PDX neurospheres. Glioma spheres were co-transduced with lentivirus-encoded shRNAs targeting DAXX (shDaxx) or shRNA Control (shLuc), and a near infrared fluorescence protein. Relative fluorescence signal was monitored by FMT. (c,e) Relative fluorescence quantification of GSC11, GSC23 and HK281 PTEN-NULL (c), and GBM6, TS765 and GBM39 PTEN-WT (e) glioma-PDX xenografts analysed by FMT imaging (*P<0.05, **P<0.001 and ***P<0.0001, one-way ANOVA). (d,f) Kaplan–Meier survival curves of mice implanted with PTEN-deficient (d) or wild-type PTEN (f) GBM-PDXs expressing shDaxx or shControl. (g–j) In vivo rescue experiments in DAXX-kd/PTEN-deficient GSC23 engrafted mice after re-expression of HA-DAXX-shRNA-resistant (shDaxx/HADAXX) or PTEN-WT (shDaxx/PTEN). (g) Representative FMT images, (h) Relative fluorescence quantification, (i) Kaplan–Meier survival curves and (j) immunoblot analysis from tissues. PTEN antibody also detects endogenous mouse-Pten in shLuc and shDaxx samples. NS: no significant differences.

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