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Figure 5 | Molecular Cancer

Figure 5

From: Panobinostat reduces hypoxia-induced cisplatin resistance of non-small cell lung carcinoma cells via HIF-1α destabilization

Figure 5

Activation of apoptosis in NSCLC cells upon co-treatment with cisplatin and panobinostat. (A) H23 cells treated for 24 hours with single substances or with combination of both were stained with Hoechst 33342 in order to determine the level of chromatin fragmentation as an indicator of apoptosis. Cells were observed under the fluorescent microscope and representative photographs were made. Note markedly increased chromatin fragmentation in co-treated cells, those effects being better visible in boxed area at higher magnification. Percentage of fragmented nuclei in relation to total number of cells is shown (three independent experiments performed in triplicates). Scale bar = 50 μm. (B) Upon treatment H23 cells were stained with propidium iodide (PI) and analyzed by FACS for the sub-G1 peak characteristic for apoptosis. Data analysis was performed by ModFit LT 3.3 software package. Representative figures (left panel) and mean values (right panel) are shown. (C, D) NSCLC cells were treated with indicated concentrations of panobinostat, cisplatin or with combination of both, harvested in RIPA buffer and cell lysates were analyzed by immunoblotting using antibodies against different apoptosis markers. Upon stripping β-actin was used as loading control. P, panobinostat (16 nM); C, cisplatin (16 μM); P + C (16 nM panobinostat + 16 μM cisplatin); NOX, normoxia; HOX, hypoxia; Cl. PARP = cleaved PARP.

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