| Objective: To investigate the effect of recombinant Newcastle disease virus expressing human IFN-?1(r L-h IFN-?1)on the proliferation,migration and invasion of lung adenocarcinoma A549 cells,and to explore its possible mechanism,which will provide a certain theoretical basis for clarifying the pathogenesis of lung cancer,and help to identify potential targets for the diagnosis and treatment of lung cancer.Methods: A549 cells were cultured in vitro,then infected by rL-hIFN-?1,Newcastle disease virus Lo Sota(NDV)or treated with PBS.Identification of successful virus infection cells was as follows: Western blot assay was used to detect the expression of NDV HN and IL-29 protein in A549 cells.The effects of r L-h IFN-?1 and NDV on the proliferation,migration and invasion of A549 cells were detected by scratch test and Transwell invasion assay.The expression levels of E-cadherin,MMP2,vimentin and certain AKT/NF-?B pathway related proteins in r L-h IFN-?1 and NDV infected A549 cells were detected by Western blot.Results: After A549 cells were infected with rL-hIFN-?1,the expression of NDV HN and IL-29 protein was stable,and it was significantly higher than that of NDV and control group.After infected with r L-h IFN-?1 and NDV,the ability of proliferation,migration and invasion of A549 cells was inhibited,and r L-h IFN-?1 is more powerful compared with the PBS group or NDV group.Compared with the PBS group and NDV group,the expression level of E-cadherin in the A549 cells was significantly increased after r L-h IFN-?1 infection,and the expression of vimentin,MMP2(66 kd/72 kd),p-AKT and P65 protein were significantly decreased(all P<0.05).Conclusion: r L-h IFN-?1 inhibited the proliferation,invasion and migration of lung adenocarcinoma A549 cells,and the mechanism may be up-regulation of E-cadherin protein expression and down-regulation of MMP2 and Vimentin protein expression by inhibiting the AKT//NF-?B signaling pathway. |
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