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Objective To investigate the effects of long non-coding RNA FEZ family zinc finger 1 antisense RNA 1(lncRNA FEZF1-AS1)on enhancer of zeste homolog 2(EZH2)in regulation of proliferation,migration,invasion and epithelial-mesenchymal transition(EMT)of pulmonary interstitial cells and its mechanism.Methods The A549 cells human lung adenocarcinoma cell line were divided into control group and model group[model cells were induced into lung interstitial cells after being treated with transforming growth factor β1(TGF-β1)20 ng/mL for 48 h].The protein expression of E-cadherin,N-cadherin and vimentin in each group was detected by Western blot.The expression of lncRNA FEZF1-AS1 and EZH2 in the two groups was detected by RT-qPCR.Cells in the trans-fection group were divided into si NC group,lncRNA FEZF1-AS1+OE vector group and si lncRNA FEZF1-AS1+OE EZH2 group.Cell proliferation was examined by CCK-8 method,cell migration was detected by cell scratch,and cell invasion was detected by Transwell assays.The protein expression of E-cadherin,N-cadherin,vimentin and EZH2 in each group was detected by Western blot.The direct binding effect of FEZF1-AS1 and EZH2 was deter-mined by RNA immuno-precipitation(RIP).Results Compared with the control group,the protein expression level of E-cadherin in the model group was significantly decreased(P＜0.05),and the protein expression of N-cadherin and vimentin was significantly increased(P＜0.05).Compared with the control group,the expression level of lncRNA FEZF1-AS1 and EZH2 genes was significantly increased in the model group(P＜0.05).Compared with si NC group,the proliferation,migration and invasion ability of si lncRNA FEZF1-AS1+OE vector group were decreased,the ex-pression of E-cadherin protein was increased while the expression of N-cadherin,vimentin and EZH2 was decreased(P＜0.05).Compared with si lncRNA FEZF1-AS1+OE vector group,the proliferation,invasion and migration of si lncRNA FEZF1-AS1+OE EZH2 group were increased(P＜0.05).E-cadherin expression was decreased,while N-cad-herin,vimentin and EZH2 expressions were increased(P＜0.05).RIP experiment further confirmed that lncRNA FEZF1-AS1 had direct binding effect with EZH2.Conclusions LncRNA FEZF1-AS1 can promote the proliferation,invasion,metastasis and EMT process of pulmonary fibrosis cells by regulating EZH2.
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Objective: To investigate the effect of astragaloside IV on tumor cellular uptake and antitumor efficacy by ginsenoside compound K (GCK). Methods: The human lung adenocarcinoma cell line A549 was prepared as an antitumor model, the cytotoxicity of the mixtures of GCK and astragaloside IV to A549 cells was determined by MTT assay, the cellular uptake of GCK was detected by fluorescence microscopy, and the intracellular GCK was determined by HPLC. The enhancement of astragaloside IV in vivo efficacy by GCK was evaluated by nude mice bearing tumor model. Results: The effect of GCK on the inhibition of A549 cell proliferation was enhanced in the presence of astragaloside IV and astragaloside IV could increase the uptake rate of GCK in A549 cells, with the proportion of astragaloside IV increasing, the cytotoxicity was significantly stronger than GCK and the uptake rate was improved. In vivo antitumor assay of mice bearing tumor indicated that astragaloside IV could enhance the antitumor efficacy of GCK. Conclusion: Preliminary results indicate that the mixture of GCK and astragaloside IV have the effect of enhancing antitumor efficacy.
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In order to investigate the inhibitory effects of Endostar(rh-endostatin,YH-16)in combination with radiotherapy on lung adenocarcinoma A549 in mice and the interaction mechanisms of combined therapy,the transplantation tumor models of A549 lung adcnocarcinoma were established.When the largest diameter of tumor reached 1.0 cm,all nude mice were randomly divided into 4 groups: Endostar group,radiotherapy group,radiotherapy plus Endostar(combined treatment)group,and control group(n=6 in each group).The largest diameter and the vertical diameter of tumor were measured at different time points.At the 16th day,mice were executed,and the tumors were applied to analysis of rate of tumor cell apoptosis,and the expression levels of basic fibroblast growth factor(bFGF)mRNA were detected by reverse transcription-polymerase chain reaction(RT-PCR)and those of vascular endothelial growth factor(VEGF)by immunohistochemistry.The results demonstrated that the rate of tumor inhibition in combined treatment group was higher than that in other groups.And the rate of tumor cell apoptosis in combined treatment group was also higher than that in other groups.Meanwhile,the levels of bFGF mRNA and VEGF expression in combined treatment group were lower than those in other groups.It was concluded that Endostar obviously enhanced the curative effectiveness of radiotherapy on lung adenocarcinoma A549 in mice.The underlying mechanisms may involve the down-regulation of bFGF mRNA and VEGF expression to inhibit angiogenesis by Endostar and the cooperative effect of Endostar and radiotherapy to synergistically promote tumor cell apoptosis.And Endostar inhibits angiogenesis by down-regulating the expression of bFGF mRNA and VEGF.