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Fig. 7 | Journal of Hematology & Oncology

Fig. 7

From: The novel thiosemicarbazone, di-2-pyridylketone 4-cyclohexyl-4-methyl-3-thiosemicarbazone (DpC), inhibits neuroblastoma growth in vitro and in vivo via multiple mechanisms

Fig. 7

Molecular mechanisms involved in the DpC-mediated anti-neuroblastoma activity. a Western analysis demonstrating that incubation of SK-N-LP neuroblastoma cells with either Dp44mT or DpC (25 μM) for 24 h/37 °C significantly: (i) reduced IĸBα levels, (ii) increased cleaved caspase 9 levels, and (iii) increased cleaved caspase 3 levels. DpC also significantly increased the phosphorylated JNK (p-JNK)/total JNK (t-JNK) ratio. Western blotting was performed as described in the “Methods.” The bands presented are representative of three repeats and have been cropped from raw data images containing all three repeats (shown in Additional file 1) for clarity (blots separated by dotted lines). b The cytotoxic effects of (i) DpC and (ii) Dp44mT on SK-N-LP cells are significantly reduced upon inhibition of the JNK, NF-ĸB or caspase (Cas) pathways, while inhibition of p38 signaling only reduced DpC cytotoxicity. SK-N-LP cells were pre-incubated for 2 h/37 °C with ERK1, p38, JNK, NF-ĸB, or Cas inhibitors prior to incubation with either DpC (25 μM) or Dp44mT (25 μM) in the presence or absence of these inhibitors for 24 h/37 °C. Cell viability was assessed using the XTT assay, as described in the “Methods .c Significantly higher levels of secreted (i) TNFα were detected in the xenografts of the DpC-treated mice (p < 0.05), while no significant changes in (ii) IFNγ or (iii) IL-10 secretion were detected. The levels of these cytokines were quantified via the ELISA assay, as described in the “Methods .” Data in graphs is presented as the mean ± SEM (n = 3). *p < 0.05; **p < 0.01; ***p < 0.001, as determined by an unpaired Student’s two-tailed t test

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