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. 2015 Jun 15;6(17):14754–14765. doi: 10.18632/oncotarget.4474

Figure 1. AICAR inhibits the growth and reduces survival of EGFR- and HER2-activated breast cancer cell lines.

Figure 1

A. MTT assay of breast cancer cell line viability after 1mM AICAR treatment for 24 hours. Data shown represent means and SEM of triplicate treatments for thirteen cell lines. B. Effect of AICAR treatment on colony forming efficiency of SKBR3, MCF7, MDA231 and HCC1806 cells. Survival differences parallel those of the MTT assay. All clonogenic assays were done in triplicate. C. Immunoblots measuring HER2 and EGFR levels in selected breast cancer cell lines. Note that cell lines sensitive to AICAR have relatively high levels of HER2, EGFR, or both. D. Flow cytometry measurements of cell-cycle distribution of propidium iodide-stained SKBR3 and MCF7 cells treated with either DMSO or 1mM AICAR for 24 hours. Presence of large sub-G1 populations in AICAR-treated cells is consistent with apoptosis. E. Western blot analysis for cleaved PARP in SKBR3 treated with indicated concentrations of AICAR (or DMSO alone) for 24 hours confirms high levels of apoptosis-mediated cell death in SKBR3 cells, but not in MCF7 cells. F. Colony forming efficiency of MCF10A cells treated with AICAR, comparing cells transfected with empty vector (pFBneo) to MCF10A clones with stable overexpression of EGFR (EGFR #7 and EGFR #9). Overexpression of EGFR in MCF10A cells results in increased sensitivity to AICAR. G. EGF treatment rescues AICAR-mediated growth inhibition of breast cancer cell lines in HCC1419 and BT474 cell lines. Representative wells from three independent clonogenic assays are shown.