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- W2366850648 abstract "Background and purpose:Proteasome inhibitors such as bortezomib,represent an interesting new class of potential anticancer drugs.In the present study,we explored the sensitivity of ovarian cancer cell line SKOV3 to paclitaxel,proteasome inhibitors and their combination,and also studied the involvement of GSK-3β/Mcl-1 signaling pathway in the regulation of apoptosis induced by those agent.Methods:Methyl thiazolyl tetrazolium (MTT)assay was applied to examine the cell viability,Annexin-V/PI apoptosis detection kit was used to determine the apoptosis rate of different groups,and western blot assay was introduced to evaluate the expression levels of phosphorylated GSK-3βand Mcl-1.Results:In the MTT assay,the cell viability ratios of combination group at serial time points from 12 to 72 hr were(65.2±5.8)%,(58.3±14.4)%,(35.3±5.0)%,(19.2±1.5)% and(11.4±2.5)%,and there were significant differences as compared to the treatment of paclitaxel alone(P0.05).After drug treatments, apoptosis rates of paclitaxel group,bortezomib group and combination group were(14.7+0.5)%,(15.1±0.8)% and (20.5±0.7)%,respectively.The rate of combination group was much higher than that in the other two groups(P0.05). Western blot assay showed that after the treatment of paclitaxel and bortezomib combination,phosphorylated GSK- 3βand Mcl-1 were significantly down-regulated(P0.05).Conclusions:The cytostatic effect of paclitaxel could be increased significantly by the combination of proteasome inhibitors like bortezomib and paclitaxel.And the GSK- 3β/Mc1-1 signaling pathway may play an important role in the molecular mechanism of apoptosis induced by the combination treatment." @default.
- W2366850648 created "2016-06-24" @default.
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- W2366850648 date "2008-01-01" @default.
- W2366850648 modified "2023-09-24" @default.
- W2366850648 title "The role of GSK-3βin apoptosis induced by proteasome inhibitors combined with paclitaxel in ovarian cancer cells and its possible mechanism" @default.
- W2366850648 hasPublicationYear "2008" @default.
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