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. Author manuscript; available in PMC: 2015 Jan 1.
Published in final edited form as: Clin Cancer Res. 2013 Oct 29;20(1):199–212. doi: 10.1158/1078-0432.CCR-13-0762

Figure 5. Cytotoxicity of Azt/nimbolide is irreversible.

Figure 5

(A) Growth assay showing viability of U87EGFRvIII cells following pre-treatment with medium (control), EtOH (control) or Azt (2μg/μl). (B) Immunoblot analysis showing activation of growth factor pathways by serum and acute inhibition of the pathways by Azt/nimbolide. Note: phosphorylation of Akt, Erk1/2 and STAT3 and RB by serum in the presence of EtOH (control) and robust inhibition of phosphorylation in the presence of Azt. Also note that mTORC1 activation, indicated by phosphorylation of S6 and 4EBP1 is unaffected by Azt. Actin was used as a loading control. Data is representative of at least three independent experiments. (C) Representative digital photograph showing tumor growth in mice injected with EtOH-pretreated (red arrowhead) or Azt-pretreated (blue arrowhead) U87EGFRvIII cells. (D) Growth of tumor xenografts in Nu/Nu mice (n=8) initiated by U87EGFRvIII cells pretreated with EtOH or Azt. Tumor volume was measured at indicated time points and the mean tumor volume was calculated. *p ≤ 0.0002.