Objective: To investigate the effect of 1

8-dimethyl-3

5

7-trinitro-2-quinolone in promoting the apoptosis of lung adenocarcinoma A549 cells

and explore its underlying mechanism.Method: The effect of 1

8-dimethyl-3

5

7-trinitro-2-quinolone on A549 cell line proliferation was detected by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay

and flow cytometry was used to determine the apoptosis rate. Protein expressions of cleaved-cysteine aspartate protease-3(Caspase-3)

B-cell lymphoma-2(Bcl-2)

Bcl-2 associated X protein(Bax)

Akt

p-Akt

forkhead bax protein O1(FOXO1)

p-FOXO1 and Bim in A549 cells were detected by Western blot.Result: The 1

8-dimethyl-3

5

7-trinitro-2-quinolone (1.25

2.5

5

10

20 mg · L-1) inhibited A549 cell proliferation in time and dose-dependent manners. The half-maximal inhibitory concentration (IC50) was 2.80

2.05 μmol · L-1

respectively at 12

24 h. Flow cytometry showed that 1

8-dimethyl-3

5

7-trinitro-2-quinolon could significantly induce apoptosis of A549.The apoptosis rate was gradually increased with the rise of drug concentration. The expressions of cleaved-caspase-3 and Bax protein were increased

while the expression of Bcl-2 were decreased. At the same time

the expressions of p-Akt and p-FOXO1 protein were increased

while the expression of Bim was decreased.Conclusion: The 1

8-dimethyl-3

5

7-trinitro-2-quinolone could induce apoptosis in A549 cells

which may be related to the phasphatidylinositol 3-kinase(PI3K)/Akt/FOXO1 signaling pathway.