The Proliferation And Mechanism Of Bovine Lactoferricin Resisting Human Lung Cancer Cells

Objective To observe the function and mechanism of bovine lactoferricin （LfcinB） onthe treatment of human lung cancer cell.Method Cultivating human lung adenocarcinoma A549cell line in vitro: theexperiment was divided into three groups: negative control group, LfcinB treatmentgroup and positive control group. Milk ferritin of antimicrobial peptides proliferationresponse was evaluated with MTT assay in human lung adenocarcinoma A549cells.Thecell cycle and apoptosis rate were determined by flow cytometry instrument. Theexpression of Bax, Bcl-2, Caspase-3mRNAwere was detected by RT-PCR, while theprotein expression of Bax, Bcl-2, Caspase-3was observed by Western blot.Result1. Compared with negative control group, different concentrations of LfcinBhave inhibition effect on A549lung cancer cell proliferation after inducing48h, theconcentration of10^-2g/L on tlactoferrin antimicrobial peptides had the highestinhibition rate.2. Compared with negative control group, different concentrations ofLfcinB role in lung cancer A549cells,24,48and72h after the G0/G1phase of thecell were slightly reduced, S phase cells gradually increased, G2/M phase of the cellslightly decreased, and in the72h is most significant （P <0.01）. LfcinB(10^-610^-2mg/ml) induced48and72h may be induced apoptosis of A549lung cancer cells.With higher drug concentration, inducing apoptosis has obvious dose effect relationship.3. RT-PCR and Western blot results demonstrated that compared with negative control group, the expression of Bax was increased with the LfcinB concentration; theexpression of Bcl-2was decreased with LfcinB concentration; and the expression ofCaspase-3was increased with the LfcinB concentration.Conclusion LfcinB could significantly inhibit human lung adenocarcinoma A549cells proliferation and blocked the cell in S phase, and induced cell apoptosis. LfcinBpromoted cells through increasing expression of Bax and decreasing the expression ofBcl-2to regulate apoptosis of A549cells whose process might be associated withcaspase activation.