Study on the role and mechanism of STAT3 and E-cadherin in epithelial mesenchymal transition of esophageal squamous cell carcinoma / 国际外科学杂志

ABSTRACT

Objective To investigate the expression and clinical pathological correlation of STAT3 and E-cadherin in esophageal squamous cell carcinoma,as well as the effect of the process in the transformation of epithelial mesenchymal transition of esophageal squamous cell carcinoma.Methods The 50 cases of esophageal squamous cell carcinoma tissues and corresponding adjacent tissues,to detect the expression of STAT3 and E-cadherin expression by RT-qPCR method in carcinoma and adjacent normal tissue expression that differential expression in mRNA level,analyzed its relationship with clinical pathological characteristics between patients;the expression of STAT3 and E-cadherin was detected by Western blotting in 4 cases of esophageal squamous cell carcinoma by simple random sampling.The author detected the expression of STAT3 and E-cadherin in three strains of esophageal squamous cell carcinoma cell lines using RT-qPCR and Western blotting,in which a high expression strains were transfected by STAT3 small interfering RNA screening,as the experimental group,using double stranded nonsense RNA transfection as the control group,detected the changes of expression level of STAT3 and E-cadherin.Detected cell migration and invasion by cell scratch test and Transwell cell invasion test in the experimental group.Measurement data were expressed by ((x) ± s),and the t test was used comparison between groups.Results In 50 cases of esophageal carcinoma,the relative expression of STAT3 was 1.87 ± 0.71,E-cadherin was 0.63 ± 0.28,in paracancerous tissue STAT3 was 0.56 ± 0.45,E-cadherin was 2.01 ± 0.68;analysis of clinical pathological features of esophageal squamous cell carcinoma showed relatively high expression of E-cadherin as relatively low expression levels of STAT3,related to the depth and lymph node metastasis in carcinoma tissues (P ＜ 0.05).Among which 4 cases were selected,the expression of STAT3 in cancer tissues higher than in corresponding adjacent normal tissues,0.28 ± 0.06 vs 0.05 ± 0.02,P ＜ 0.05,and the expression of E-cadherin in cancer tissues was significantly lower than that in adjacent normal tissues,0.27 ± 0.07,0.59 ± 0.09,P ＜ 0.05.The high expression of EC109 from carcinoma cell lines was as experimentation of esophageal squamous cell,RT-qPCR results showed that the expression of STAT3 was significantly decreased in small interfering RNA transfection group than the control group 0.85 ± 0.24 vs 3.01 ± 0.20,P ＜ 0.05,while up-regulation of E-cadherin protein expression,2.69 ± 0.29 vs 0.36 ± 0.16,P ＜ 0.05;Western blotting detection,compared with the control group,the expression of STAT3 protein was successfully inhibited after transfection of STAT3 small interference RNA fragment (0.09 ±0.04 vs 0.32 ±0.18,P ＜ 0.05),while the expression of E-cadherin was up-regulated in EC109 cells (0.75 ±0.11 vs 0.15 ±0.05,P ＜0.05).After downregulation of STAT3 expression,cell scratch test and transwell cell invasion test showed that the migration and the number ofinvasion cell number of STAT3 small interfering RNA transfection group in esophageal squamous carcinoma cell line EC109 compared with the control transfected double-stranded non-sense RNA group were decreased,so the downregulation of STAT3 expression after migration,invasion ability were weakened (P ＜ 0.05).Conclusion In esophageal squamous cell carcinoma,STAT3 transcription factor can mediate E-cadherin expression and affect epithelial mesenchymal transition phenotype,thereby affecting tumor migration and invasion.