目的:探讨X连锁凋亡抑制蛋白(XIAP)在口腔鳞癌中的表达及其与患者预后之间的关系.方法:运用免疫组化技术检测52例口腔鳞癌组织标本中XIAP蛋白的表达情况,评价其表达水平和患者各临床病理参数及患者预后之间的关系.结果:纳入研究的52例临床标本中XIAP阳性表达14例(27%).XIAP表达水平与病理分级相关,并且和患者预后显著相关.结论:XIAP蛋白可能参与了口腔鳞癌的发生发展,并且与患者预后密切相关.
Objective:To detect the progress of epithelial-mesenchymal transition(EMT) in esophageal squamous carcinoma cells(ESCC) TE-1 which was treated with ionizing radiation,and explore the underlying mechanisms.Methods:After treated with different intensity of ionizing radiation (0,2,4,8 Gy),realtime PCR was used to detect the mRNA expression of Snail 1 and AP-1 in TE-1 cells.Western blot was used to measure the protein expressions of Snail 1,Slug,E-cadherin and Vimentin.The protein levels of Ecadherin and Vimentin was verified by immunofluorescence.The ability of migration was measured by wound healing test and Transwell inserts.Dealing with ionizing radiation (4 Gy) and/or DAPT the inhibitor of Notch signaling pathway,the expression levels of Notch 1,NICD,Hes 1 and MMP-9 proteins were measured by Western blot.Results:After treated with ionizing radiation,TE-1 cells showed the up-regulation effect of the transcription factors of EMT(Snail 1,Slug,AP-1),mesenchymal marker(Vimentin) and metastasis related protein (MMP-9),meanwhile the down-regulation effect of epithelial marker(E-cadherin).and when dealing with 4 Gy radiation,the changes was significant (P <0.01).Ionizing radiation accelerated the transfer ability of TE-1 (P < 0.05).By up-regulating the expression levels of Notch 1/NICD/Hes 1 signaling pathway,ionizing radiation promoted EMT related protein expressions (P < 0.01).Conclusion:The ionizing radiation strengthens EMT,thereby induces metastasis,by activating Notch signaling pathway.
OBJECTIVETo investigate the role of interlukin-23 (IL-23) in the invasion of human esophageal squamous cell carcinoma (ESCC) cells and the related mechanism.METHODSIL-23 expression in tumor and adjacent tissues from 10 ESCC patients were detected by immunohistochemistry. Real-time fluorescent PCR was used to examine the expressions of Notch1 and Foxn4 mRNAs in different concentration IL-23-treated TE-1 cells. After Notch pathway was blocked with γ-secretase inhibitor DAPT, expressions of Notch intracellular domain (NICD), Delta-like 4 (DLL4), hairy enhancer of split 1 (Hes1), matrix metalloproteinase 9 (MMP-9) in IL-23-treated TE-1 cells were measured by Western blotting. And the migration of IL-23-treated TE-1 cells was studied by TranswellTM migration assay.RESULTSCompared with adjacent tissues, IL-23 was highly expressed in ESCC tissues. IL-23 treatment up-regulated significantly the expressions of NICD, DLL4, Hes1 and MMP-9 in TE-1 cells. The blockade of Notch1 pathway inhibited the expressions induced by IL-23. Migration assay revealed that IL-23 treatment significantly enhanced the migration of TE-1 cells.CONCLUSIONIL-23 could promote migration of human ESCC cells by activating DLL4/Notch1 signaling pathway.