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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 transfection 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 determined 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 expression 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-cadherin, 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.

The stress corrosion cracking (SCC) behaviors of X100 pipeline steels with different heat-treated microstructures in carbonate/bicarbonate solution at various potentials were investigated in this study. Several analyses were performed using electrochemical measurements, slow strain rate tensile (SSRT) tests, scanning electron microscopy (SEM), and electron back-scattered diffraction (EBSD). The results showed that the SCC susceptibilities of heat-treated microstructures increase as the cathodic potential shifts from −850 to −1200 mVvsSCE. At a weak cathodic potential, the different microstructures show clear SCC sensitivity, showing that hydrogen cannot be ignored in this circumstance when the alkaline environment is not considered seriously. At a mild cathodic potential, hydrogen sensitivity controls SCC behavior, but at a larger negative potential, both electrochemical effect and hydrogen sensitivity influence SCC behavior. The SCC cracks propagate along the high angle grain boundary (HAGB) at open circuit potential (OCP) and as the applied potential is adjusted negatively, the cracks would either follow low angle grain boundary (LAGB), HAGB or random orientation propagation paths. The synergistic influence of dislocation, grain boundary, grain size, martensite/austenite (M/A) island, and carbide controls the SCC process of the X100 pipeline. SCC susceptibility was shown to be high in microstructures with coarse grain and high dislocation density, whereas grain boundaries such as the martensite/austenite (M/A) island and carbide offer sites for SCC initiation.