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. 2015 Sep 24;5:14273. doi: 10.1038/srep14273

Figure 2. M1 macrophage CM reducing cell viability and enhancing drug sensitivity of lung cancer cells.

Figure 2

(A) Evaluation of A549 lung cancer cell viability after culturing with macrophage CM for 5 days by counting cells. *P < 0.05 (mean ± SD, n = 3). Experiments were performed in three independent triplicates. Each value of bar is presented as the average of 9 assays. (B) Proliferation of long-term-cultured A549 cells, determined by the MTT assay. *P < 0.05 (mean ± SD, n = 3) Experiments were performed in triplicate. (C) Apoptosis of A549 cells after treatment with macrophage CM for 5 days. Cell apoptosis was determined by flow cytometry with annexin V/PI-staining. Data were confirmed in three independent experiments. (D) Cell cycle distribution of CM-treated A549 cells determined by flow cytometry with PI-staining. The sub-G1 population corresponds to apoptotic cells.(E) Cellular senescence of CM-treated A549 cells assessed by counting β-galactosidase-positive cells. *P < 0.05 (mean ± SD, n = 3). Experiments were performed in triplicate. (F) The impact of macrophage subtypes on drug responsiveness. Long-term–cultured A549 cells were treated with the indicated concentrations of cisplatin. *P < 0.05 (mean ± SD, n = 3), compared with the M0 treatment. Experiments were performed in triplicate.