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Table 1 Effect of MEK162/BKM120 combination therapy on human non-small cell lung carcinoma (NSCLC) H1975, H460, and A549 cell cycle distribution

From: Dual targeting of MEK and PI3K effectively controls the proliferation of human EGFR-TKI resistant non-small cell lung carcinoma cell lines with different genetic backgrounds

Group Cell cycle distribution (%)
G0/G1 S G2/M
H1975 cells    
Control 60.3 ± 3.6 31.5 ± 4.8 8.2 ± 5.5
BKM120 78.4 ± 3.5* 18.9 ± 8.4 2.7 ± 1.8
MEK162 72.6 ± 7.7* 21.1 ± 6.8 6.3 ± 2.3
BKM120 ± MEK162 85.7 ± 5.5**##@@ 10.6 ± 2.1 3.7 ± 2.4
H460 cells    
Control 55.9 ± 4.6 33.5 ± 4.8 10.6 ± 5.9
BKM120 72.4 ± 2.5* 24.9 ± 2.4 2.7 ± 1.1
MEK162 74.6 ± 5.4* 20.3 ± 6.8 5.1 ± 1.4
BKM120 ± MEK162 91.8 ± 6.9**##@@▲ 6.6 ± 2.1 1.6 ± 0.8
A549 cells    
Control 62.8 + 3.5 26.5 + 6.8 10.7 + 5.1
BKM120 76.4 + 5.5*& 18.9 + 8.4 4.7 + 4.8
MEK162 77.9 + 6.7*& 15.8 + 3.8 6.3 + 2.9
BKM120 + MEK162 88.6 + 6.6**##@@& 9.2 + 3.8 2.2 + 1.2
  1. H1975, H460, and A549 cells were treated with 1 μM MEK162 (MEK inhibitor) or 5 μM BKM120 (PI3K inhibitor) alone or in combination for 48 h. Control cells were treated with DMSO (0.05%). After treatment, the cells were stained with propidium iodide (PI) and analyzed by flow cytometry. Each value represents mean ± standard deviation (SD) obtained from three independent experiments
  2. *P < 0.05 vs. Control; #P < 0.05 vs. BKM120; @P < 0.05 vs. MEK162; P < 0.05 vs. H1975 cells; &P < 0.05 vs. H460 cells under the same cell cycle phase and the same drug treatment