TNF enhances dose‐dependent cell death following doxorubicin‐induced DNA damage with minimal affect on dose‐dependent cell‐cycle arrest. TNF enhances dose‐dependent.

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TNF enhances dose‐dependent cell death following doxorubicin‐induced DNA damage with minimal affect on dose‐dependent cell‐cycle arrest. TNF enhances dose‐dependent cell death following doxorubicin‐induced DNA damage with minimal affect on dose‐dependent cell‐cycle arrest. (A) Representative scatter plots for cleaved caspase‐3 and cleaved PARP as measured simultaneously by flow cytometry in single cells, for all six treatment conditions, at 12 h following treatment. (B) Apoptosis in treated cell populations (percentage of the cell‐population staining positively for both apoptotic markers cleaved caspase‐3 and cleaved PARP), for all six treatment conditions investigated at 6, 12, 24, and 48 h following treatment. (C) Representative cell‐cycle profiles based on PI staining of DNA content for cells exposed to 0, 2, or 10 μM doxorubicin +/− TNFα at 6, 12, 24, and 48 h following treatment. (D) Quantification of the percentage of the treated cell populations in the G1 (a), S (b), G2/M (c), and pHH3+/M (d) phase of the cell‐cycle, and the sub‐G1 population (e) at 6, 12, 24, and 48 h following each treatment. (B, D) Mean values from n⩾4 independent experiments; error bars denote standard error of the mean. All measurements of cell‐cycle stage and apoptosis represent ‘window’ measurements that do not reflect the cumulative fraction of the initial population, but rather the fraction of the population that is still measurable at the indicated time point. For example, apoptosis measurements at later time points will not include cells that have died and disintegrated between the time of treatment and the time of measurement. Source data is available for this figure in the Supplementary Information. Andrea R Tentner et al. Mol Syst Biol 2012;8:568 © as stated in the article, figure or figure legend