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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
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BMC Pulmonary Medicine

ISSN: 1471-2466

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