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Lung cancer is the leading cause of cancer-related deaths worldwide.Despite the development and use of several targeting drugs for lung cancer therapy,the five-year survival rate has remained as low as 15%for the past three decades.Cisplatin-based chemotherapy is considered the first-line therapeutic strategy for lung cancer.However,developments of chemoresistance is a major obstacle for the successful treatment.Therefore,the development of novel therapy against cisplatin-resistance lung cancer is imperative.Photodynamic therapy(PDT),which is a non-invasive combinatorial therapeutic modality using light,photosensitizer(PS)and oxygen,may provide an unprecedented tool to develop more effective treatments.To provide experimental basis for its application in cisplatin-resistance lung cancer,we will discuss the biological effects of MPPa-photodynamic therapy in human cisplatin-resistance lung cancer cells in this article.Human cisplatin-resistance lung cancer cells A549/DDP were co-cultured with MPPa(0,1,2,4,8,16μmol/L)and exposed to light(0,0.6,1.2,2.4,3.6,4.8J/cm2),and cell viability was determined with CCK-8assay.Flow cytometry was used to detect apoptosis,DCFH-DA staining was employed to observe reactive oxygen species(ROS),and Western blot was used to detect the expressions of B-cell lymphoma-2(Bcl-2)protein and Bcl-2associated X protein(Bax).The proliferation of A549/DDP cells was suppressed by PDT.The apoptotic rate in the PDT group was significantly higher than that in the control,MPPa or light group(P<0.05).The level of ROS was increased.The expression of Bax was increased,and that of Bcl-2was decreased.MPPa-photodynamic therapy can significantly suppress cell viability,and induce apoptosis in human cisplatin-resistance lung cancer cells.

This study aims to explore the temporal pattern of DNA breaks induced by nanosecond electric pulses (nsEP) in cisplatin-sensitive and cisplatin-resistant human ovarian cancer cells. Human ovarian cancer cells A2780 (cisplatin-sensitive subline) and C30 (cisplatin-resistant subline) were exposed to nsEP. Sham exposed groups were shame exposed to nsEP. Cell viability was determined using CCK-8 assay after 0 h, 4 h, 8 h, 12 h and 24 h, respectively, and the percentage of dead cells was calculated. The DNA break was detected with the alkaline single cell gel electrophoresis (comet assay), and the 75th percentiles of TL (tail length), TM (tail moment) and OTM (Olive tail moment) were measured. Cell viability displayed an early decrease and late increase, with the valley value seen at 8 h. Percentages of cell death and comet-formed in A2780 cells were higher than those in C30 cells (P < 0.05) at 8 h, respectively. TL, TM and OTM in C30 cells were less than those in A2780 cells (P < 0.05). The percentage of comet-formed correlated with that of cell death in either A2780 (r = 0.997, P < 0.05) or C30 (r = 0.998, P < 0.05) cells. DNA breaks induced by nsEP in cisplatin-sensitive cells differred from that in resistant cells, and DNA break resulted in fraction of cell death.

Recombinant human interleukin-1 receptor antagonist was expressed in E. coli as an insoluble inclusion body. The inclusion body was dissolved in the 8 M urea and then the solution was diluted untill the concentration of urea became 2 M. By ion exchange chromatography the protein in the solution of 2 M urea was refolded and purified. At last the purity of product is more than 95% and its bioactivity is more than 1 x 10(5) IU/mg while it has little endotoxin. Western-Blotting also indicates that recombinant protein can react with antibodies against anti-hIL-1ra.