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Objective @#To investigate the effect of Rotundic acid (RA) on proliferation，migration and invasion a- bility of human lung adenocarcinoma cells as well as its possible mechanisms．@*Methods @#Human lung adenocarci- noma A549 and PC9 cells were divided into control group，blank control group，solvent group and 20，40，60，80 μmol / L RA groups．CCK-8 assay and scratch assay were used to detect the proliferation and horizontal migration of human lung adenocarcinoma cells．Transwell migration assay and Transwell invasion assay were used to detect the longitudinal migration and invasion ability of A549 and PC9 cells in each group．The protein expression levels of ja- nus kinase 2 (JAK2) and signal transducer and activator of transcription 3 ( STAT3) in the supernatants of A549 and PC9 cells were detected by ELISA．The mRNA expression levels of JAK2 and STAT3 were detected by RT- PCR. Statistical analysis was made on the differences among groups in each index. @*Results @#After RA treatment on human lung adenocarcinoma cells ，compared with the control group ，the proliferation activity of A549 and PC9 cells in the experimental groups decreased (P＜0. 05) ，the number of cells crossing polycarbonate membrane and matrix glue decreased (P＜0. 05) ，the expression of JAK2 and STAT3 proteins in cell supernatant decreased (P < 0. 05) ，and the mRNA expression of JAK2 and STAT3 decreased (P＜0. 05) ．The decrease of the above indices was concentration-dependent and had statistical significance (P＜0. 05) ．Compared with the control group，the pro- liferation activity of A549 and PC9 cells in the solvent group showed no significant difference．@*Conclusion @#RA may inhibit the proliferation，migration and invasion of human lung adenocarcinoma A549 and PC9 cells in vitro， possibly through the inhibition of JAK2 / STAT3 pathway.
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[ ABSTRACT] AIM:To study the effect of rapamycin ( Rap) on the proliferation, invasion, adhesion, apoptosis and autophagy of human adenocarcinoma A549 and resistant A549/DDP cells treated with cis-diamminedichloroplatinum ( DDP) .METHODS: Human adenocarcinoma A549 and resistant A549/DDP cell lines were cultured.The inhibitory effects of Rap alone or combined with DDP on A549 and resistant A549/DDP cells were detected by MTT assay.The in vitro invasion abilities of the 2 cell lines treated with Rap alone or combined with DDP were detected by Transwell methods. The in vitro adhesion abilities of the 2 cell lines treated with Rap alone or combined with DDP were detected by adhesion experiments.The apoptosis of A549 and resistant A549/DDP cells induced by Rap alone or combined with DDP was ana-lyzed by flow cytometry.The cell autophagy marker proteins beclin-1 and LC3 in A549 and resistant A549/DDP cells trea-ted with Rap alone or combined with DDP were detected by Western blotting.RESULTS:Compared with Rap or DDP a-lone group, the combination of Rap and DDP significantly inhibited the proliferation, invasion and adhesion of A549 and resistant A549/DDP cells in vitro, and promoted the cell apoptosis and autophagy marker proteins beclin-1 and LC3 expres-sion ( all P<0.05) .CONCLUSION:Rap enhances the effect of DDP through promoting the cell autophagy, thereby in-hibiting the proliferation, invasion and adhesion of A549 and resistant A549/DDP cells and inducing the cell apoptosis with a synergistic effect.
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Objective To investigate the changes of telomerase activity after knocking down endogenous expression of T-STAR (testes-signal transduction and activator of RNA) gene in human lung adenocarcinoma cell line A549 by antisense strategy. Methods The mRNA and protein expression of T-STAR gene were determined by RT-PCR and Western blotting, and the telomerase activity was measured by PCR-ELISA, after transfection of T-STAR antisense gene into A549 cells with lipofectamine. Sense pcDNA-STAR and blank pcDNA3.1 transfection served as control. Results The expression of T-STAR gene was significantly inhibited at mRNA and protein level, and the telomerase activity was significantly decreased. Conclusion The down-regulation of telomerase activity may result from inhibition of T-STAR gene expression in lung adenocarcinoma A549 cells.
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Objective To explore the molecular mechanism of Qingjin Desheng Tablets on inhibiting the growth of lung cancer cells and to supply experimental evidences for Chinese herbal medicine preventing and curing lung cancer in clinical application .Methods Immunohistochemistry staining was used to detect the activity of telomerase and the expression of bcl-2 and bax in human lung adenocarcinoma cells after treated with serum containing Qingjin Desheng Tablets.Results The activity of telomerase was inhibited significantly and the positive rate of bcl-2 protein reduced,and the positive rate of bax2 increased in human lung adenocarcinoma cells after 72 hour-treatment with the serum containing Qingjin Desheng Tablets.Conlusion Qingjin Desheng Tablets exert the anti-tumor action through inhibiting the activity of telomerace and modulating the expression of bcl-2 and bax protein.
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Objective To explore the sensitization effect of insulin to chemotherapy as a metabolic promoter on human lung adenocarcinoma cells A549.Methods The sensitivity of human adenocarcinoma cells A549 to DDP was observed by MTT methods,and IC30 values of the cells were calculated.The optimal concentration of insulin to promoting A549 cells' growth was determined by MTT assay.The A549 cells were pretreated with insulin of various concentrations for different time period,and then the cell sensitivity to DDP was evaluated with MTT assay.Flow cytometry was used to study the cell cycle distribution of the A549 cells treated with insulin.Results The IC30 value of DDP was about 36.87?g/ml.It was found that the cell growth was significantly promoted with pretreatment of insulin at the concentration of 4~16mU/ml for 8~16 hours.Insulin enhanced the inhibitory effect of DDP(36.87?g/ml)on cell proliferation when human lung adenocarcinoma cells A549 were treated with insulin(2.0~16.0mU/ml;8~16h)as indicated by MTT assay(P