Objective:To investigate the effect of Bortezomib on human cervical cancer SiHa cell transplanted tumor in nude mice and its relationship with Janus kinase 2(JAK2)and signal transducer and activator of transcription 3(STAT3)expression.Methods:The model of human cervical cancer SiHa cell transplanted tumor in nude mice was established,and the mice were randomly assigned into the control group(n=8),and the administration group(n=8).The changes of body mass and transplanted tumor volume in nude mice were monitored.The nude mice were sacrificed at the end of trial,and the tumors were removed for calculation of tumor inhibition rate.The tumor tissues were stained with HE.The gene expressions of JAK2 and STAT3 were detected by RT-PCR.The protein expressions of JAK2,STAT3,phosphorylated JAK2,and phosphorylated STAT3 were determined by western blot.Results:(1)There was no significant difference in weight of nude mice between the two groups before and after intervention 2 weeks,but the weight of nude mice in the administration group was significantly lower than that in the control group at 3 and 4 weeks after intervention(P<0.05);(2)The tumor volume of the administration group was significantly smaller than that in the control group(P＜0.05),and the tumor suppression rate in the administration group was 21.4%;(3)In the control group,tumor cells invaded the region of connective tissue and adipose tissue.But in the administration group,the boundary between tumor tissue and connective tissue,adipose tissue was complete and regular;(4)There was no significant difference in the gene expression of JAK2 and STAT3 between the two groups(P>0.05);(5)There was no significant difference in the protein expression of total JAK2 and STAT3,but the protein expression of phosphorylated JAK2 and STAT3 in the administration group was significantly lower than that in the control group(P>0.01).Conclusion:Bortezomib can inhibit the growth and invasion of human cervical cancer SiHa cells trans-planted tumor in nude mice,which may reduce the activity of JAK2/STAT3 signaling pathway by inhibiting the expression of phosphorylated JAK2 and STAT3 proteins.
维普
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