Abstract Objective: To establish a model of incomplete ablation in nude mice with hepatocellular carcinoma (HCC) and to evaluate heat shock protein (HSP) expression and autophagy and their correlation. Materials… Click to show full abstract
Abstract Objective: To establish a model of incomplete ablation in nude mice with hepatocellular carcinoma (HCC) and to evaluate heat shock protein (HSP) expression and autophagy and their correlation. Materials and methods: In the first stage, 12 nude mice with HCC were randomly divided into two groups (n = 6). A sham puncture operation was performed for one group, and palliative laser ablation was performed for the other group. All mice were sacrificed after 18 h, and HSP expression, autophagy, and apoptosis were assessed. In the second stage, 16 nude mice with HCC were randomly divided into two groups (n = 8). One group was given an HSP90 inhibitor before the operation, and the other group was given dimethyl sulfoxide (DMSO) as a control. HSP expression, autophagy and apoptosis were assessed for the two groups after palliative laser ablation. Results: In the incomplete ablation model, using nude mice with HCC, HSP90, HSP70, and HSP27 expression was up-regulated, Akt and mTOR phosphorylation was enhanced, autophagy was decreased, and apoptosis was increased. After administration of the HSP90 inhibitor, HSP90, P-Akt, and P-mTOR expression was decreased, autophagy was increased, and apoptosis was further increased. Conclusion: Autophagy was decreased in the incomplete ablation model and might be inversely correlated with HSP expression. It is suggested that the HSP90/Akt/mTOR pathway is involved in signal transmission between autophagy and HSPs.
               
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