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Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: The HIF1α-PDGFD-PDGFRα axis controls glioblastoma growth at normoxia/mild-hypoxia and confers sensitivity to targeted therapy by echinomycin

Fig. 7

Overexpression of PDGF-D increases angiogenesis and sensitivity to LEM treatment in immunocompetent mice. A Anti-V5 tag antibody detected the ectopic expression of PDGF-D or PDGF-D-dCUB in the mouse GBM line GL261 expressing luciferase. B-F C57BL/6 were orthotopically transplanted with GL261 cells lentiviral-transduced by vector control, PDGF-D-dCUB, or PDGF-D, as indicated in the headings, and treatment with vehicle or LEM was administered as described in methods. Bioluminescence imaging is shown for the different groups (B). The survival of mice receiving vector-, PDGF-D-, or PDGF-D-dCUB-transduced GL261 cells is shown in (C). Experimental design and treatment schedule with LEM is depicted in (D), and the Kaplan-Meier survival curves of mice receiving vector- or PDGF-D-transduced GL261 are shown in (E) and (F), respectively, comparing survival among vehicle or LEM-treated groups. G Representative immunofluorescent staining of vector- (GL261-V) or PDGF-D-transduced (GL261-PDGF-D) brain tumor tissue sections are shown from PBS-perfused recipient mice after staining for CD31 or PDGFRα. H Summary of the underlying mechanism

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