ABSTRACT
The damage behaviors of polyimide fiber after 150 keV proton irradiation and the synergistic effect of proton irradiation and strain were investigated. Changes in the mechanical properties, free radicals, element content, and element chemical state of the polyimide fiber before and after 150 keV proton irradiation were investigated. The results showed that the tensile strength and elongation at break of the material decreased significantly after proton irradiation. The synergistic effect of proton irradiation and strain weakened the reduction of mechanical properties caused by single proton irradiation. After proton irradiation and the combination of proton irradiation and strain, pyrolytic carbon free radicals were generated. According to XPS analysis, the proton-irradiated polyimide fiber underwent complex denitrification and deoxygenation reactions, and carbon enrichment appeared on the surface of the material.
ABSTRACT
AIM: To investigate the role of HGF/c-Met signaling pathway in crizotinib-induced apoptosis of different lung carcinoma cell lines and to analyze its potential regulatory mechanisms .METHODS: EML4-ALK positive cell line H2228, c-Met proliferation cell line H1993 and control cell line A549 were treated with crizotinib at different doses for different time periods .The viability of the cell lines was measured by MTT assay .The apoptosis was analyzed by flow cytometry with PI staining.The protein levels of MET and phosphorylated MET (p-MET) of HGF/c-Met signaling pathway as well as its down-stream key proteins AKT , ERK, p-AKT and p-ERK in the cell lines before and after crizotinib treatment were examined by Western blot .RESULTS:The growth of H1993, H2228 and A549 cell lines was inhibited after crizoti-nib treatment for 72 h in a dose-dependent manner .Apoptotic rates of H1993 cells and H2228 cells were increased with the crizotinib concentration and exposure time .Down-regulation of p-MET, p-AKT and p-ERK at protein levels in H1993 cells and H2228 cells after exposure to crizotinib for 72 h was confirmed by Western blot .No obvious change of the related-pro-teins of HGF/c-Met signaling pathway was found in A 549 cell line.CONCLUSION: HGF/c-Met signaling pathway may contribute to crizotinib-induced apoptosis of H1993 cells and H2228 cells, which provides the experimental basis for MET-targeting treatment of lung cancer .
