Objective: To investigate the effect of 1

2:5

6-dianhydrogalactitol (DAG) in vitro proliferation and apoptosis of human lung cancer cell lines. Method: Cell counting Kit-8(CCK-8) method was used to measure the inhibition rate of DAG in vitro proliferation of 11 kinds of human lung cancer cells:Calu-1

NCI-H1650

NCI-H358

NCI-H1299

HCC827

PC-9

A549

NCI-H661

NCI-H292

95-D and NCI-H446

then cells with higher inhibition rates and good growth conditions were selected for subsequent research. Trypan blue exclusion method was used to detect the cell survival rate after treatment by DAG. Transmission electron microscope was used to observe the changes in submicroscopic structure after apoptosis. Real-time PCR was used to detect the effect of DAG on Bax

Bcl-2 and Caspase-3 mRNA expression levels within the cells. Result: DAG significantly inhibited the 11 kinds of human lung carcinoma cell lines with a good concentration-effect relationship. As compared with the blank group

the inhibition rate on cells proliferation was increased with the increase of dose (P < 0.01). Trypan blue exclusion results showed that

with the increase of drug concentrations

the count of cells in blue (dead cells or cells with damaged membrane) was increased. Transmission electron microscope results indicated that

after 48 h treatment

apoptotic cells were rounded overall

microvilli fell off

with karyopyknosis and margination

heterochromatin with high electron density in the nucleus was condensed into lumps and aggregated on nuclear membranes

with mitochondrial swelling and vacuolar degeneration within cells. Real-time PCR results indicated that the expression of pro-apoptosis gene Bax was up-regulated

expression of anti-apoptosis gene Bcl-2 was down-regulated

and Caspase-3 was activated. Conclusion: DAG can inhibit the human lung carcinoma cells growth and induce their apoptosis

and the potential mechanism may be associated with up-regulating the expression of Bax

down-regulating the expression of Bcl-2 and activating Caspase-3.