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Figure 1 | Molecular Cancer

Figure 1

From: Concordant and opposite roles of DNA-PK and the "facilitator of chromatin transcription" (FACT) in DNA repair, apoptosis and necrosis after cisplatin

Figure 1

Dual role of DNA-PK in response to cisplatin. A. Cisplatin-induced phosphorylation of H2AX is regulated by DNA-PK. DNA-PKcs (PKcs) or control (ctr) shRNA-expressing A2780 cells were treated with 100 μg/ml cisplatin (CIS) for 0, 1 or 2 hours (hrs). DNA-PKcs and β-actin were analyzed in whole cell lysates by immunoblotting. γH2AX and H2A were analyzed in chromatin fractions (chrom). B. Levels of cisplatin-induced PARP-1 cleavage after silencing DNA-PKcs expression in A2780 cells. DNA-PKcs, PARP-1, and β-actin were analyzed in whole cell lysates of cells treated with 100 μg/ml cisplatin for 0, 4 or 6 hrs by immunoblotting. C. DNA-PK inhibition sensitizes cancer cells to cisplatin. Control and DNA-PKcs shRNA-expressing A2780, MDA-MB-231 and HEK293T cells were treated with increasing concentrations of cisplatin. IC50 values at 24 hrs are shown. Results represent the mean ± s.e.m. of five independent experiments. For comparisons of control and DNA-PKcs depletion within cell lines, p < 0.01.

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