Expressions And Significance Of STAT3, Survivin And SOCS3in Esophageal Cancer

Objective： Esophageal cancer was one of the most common gastrointestinalcancers, and significant efforts had been devoted to early detection, early diagnosis andearly treatment. In recent years, accumulating evidence indicated that oncogenesis ordevelopment was associated with a series of changes in oncogenes, anti-oncogenes andother genes, which leaded to pathophysiological changes, including uncontrolled cellproliferation and inhibition of apoptosis. And the abnormal genes and proteins were keyplayers in the initiation and progression of esophageal cancer. By investigating theexpressions of signal transducer and activator of transcription3(STAT3), survivin andsuppressors of cytokine signaling3（SOCS3）in esophageal cancer, we aimed to analyzetheir relationship with clinical characteristics and explore the pathogenesis aboutesophageal cancer in which their potentially participated for early diagnosis and providea scientific basis for treatment.Methods：Immunohistochemistry was used to determine the expressions of STAT3,survivin and SOCS3in64esophageal cancer specimens,34dysplasia specimens and31matched adjacent non-cancerous tissue specimens.Results：1. Expressions of STAT3, survivin, SOCS3in esophageal cancer, dysplasia andadjacent non-cancerous tissuesThe expression rates of STAT3and survivin in adjacent non-cancerous tissue,dysplasia and esophageal cancer gradually increased, respectively, STAT3:38.71%,64.71%,82.81%; survivin:25.81%50.00%,73.44%, and differences between thegroups were statistically significant (all P <0.05). The expression of SOCS3in esophageal cancer tissue was low and the expressionrates were35.94%and55.88%in esophageal cancer and dysplasia tissue, respectively,while80.65%in adjacent non-cancerous one. Both difference of expression ratesbetween esophageal cancer and adjacent non-cancerous tissue and that betweendysplasia and adjacent non-cancerous tissue were statistically significant (both P <0.05),however, there was no difference between the expression rates of esophageal cancer anddysplasia tissue (P=0.058>0.05).2. The relationships between STAT3, survivin, SOCS3and clinical characteristicsof esophageal cancerThe expression of STAT3in esophageal cancer had no significant correlation withsex, age, tumor location, tumor size, tumor differentiation, lymph node metastasis andadjacent structures invasion, but had significant correlation with invasion depth andclinical stage (p<0.05). And with the increase in the depth of invasion and clinicalstaging, the expression rates of STAT3protein increased. The expression of survivin inesophageal cancer had no significant correlation with sex, age, tumor location, tumorsize, tumor differentiation, invasion depth and adjacent structures invasion, but hadsignificant correlation with clinical stage and lymph node metastasis (p<0.05). And withincreasing clinical stage and occurrence of lymph node metastasis, the expression ratesof survivin protein increased in esophageal cancer. The expression of SOCS3inesophageal cancer had no significant correlation with sex, age, tumor location, tumorsize and tumor differentiation, but had significant correlation with lymph nodemetastasis, adjacent structures invasion, invasion depth and clinical stage (p<0.05). Andwith the occurrences of lymph node metastasis and adjacent structures invasion, andwith the increase in the depth of invasion and clinical staging, the expression rates ofSOCS3protein decreased.3. Correlations of expressions of STAT3, survivin and SOCS3protein inesophageal cancerThe expression of STAT3was positively correlated with survivin (r=0.570; P=0.000), but negatively with SOCS3(r=-0.349; P=0.005) in esophageal cancer. Conclusion：1. The over-expressions of STAT3and survivin proteins and the down-regulatedexpression of SOCS3protein are correlated with the tumor initiation of esophagus.2. The expression of STAT3was correlated with invasion depth and clinical stageand the expression of survivin was correlated with lymph node metastasis and clinicalstage, while SOCS3with lymph node metastasis, adjacent structures invasion, depth ofinvasion and clinical staging.3. The current results indicated that the three proteins were expected to providenew ideas to the early diagnosis and developing treatment of esophageal cancer.