Fig. 4From: Selinexor versus doxorubicin in dedifferentiated liposarcoma PDXs: evidence of greater activity and apoptotic response dependent on p53 nuclear accumulation and survivin down‐regulationInduction of apoptosis by selinexor and doxorubicin in DDLPS models. a, Western blot analysis of survivin, p53, p21, and cleaved caspase 3 on tumors obtained from untreated (Ctrl) and selinexor- or doxorubicin-treated mice at different intervals from the end of treatment. The expression of autophagy (LC3B) and senescence (p16) markers was also assessed. A representative blot of three independent experiments is shown. For each protein, band intensity was quantified using Image J normalized to loading control reported below and referred to respective untreated control. The band intensity of LC3B-I and LC3B-II were quantified separately (above and below, respectively). b, Cleaved caspase-3 immunostaining of tumors obtained from untreated (Ctrl) and selinexor- or doxorubicin-treated mice at the end of treatments (upper panel) and quantification of the percentage of cleaved caspase-3 positive cells (lower panel). c, Flow cytometric assessment of TUNEL-positive cells after 72 h exposure to equimolar concentration of drugs in DDPLS cells (upper panel) and quantification of TUNEL-positive cells (lower panel). Results represent the mean values ± SD of 3 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.005Back to article page