Imatinib abrogates doxorubicin resistance, in part, by potentiating doxorubicin-mediated G2/M arrest.

<p>(<b>A–C</b>) Proliferation was assessed in treated cells (72 h) by tritiated thymidine assay. Representative dose response curves (<b>A, B, left</b>) and Mean±SEM for 3 independent experiments (<b>A–C, right</b>). Some error bars are too small to visualize. (<b>C</b>) CI values: Dox(0.015 µM)+imatinib(2 µM) = 0.9±0.14; Dox(0.015 µM)+imatinib(5 µM) = 0.67±0.07; Dox(0.015 µM)+imatinib(10 µM) = 0.5±0.06; Dox(0.03 µM)+imatinib(2 µM) = 0.8±0.11; Dox(0.03 µM)+imatinib(5 µM) = 0.5±0.13; Dox(0.03 µM)+imatinib(10 µM) = 0.36±0.18. (<b>D, E</b>) Asynchronous drug-treated cells (72 h) were analyzed by FACS. Experiments were performed ≥3 times, and representative cell cycle distributions are shown. Mean±SEM for 3 independent experiments is shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0055509#pone.0055509.s004" target="_blank">Figure S4E</a>. **<i>p</i>≤0.01, ***<i>p</i><0.001 (see methods).