| Objective: Cancer is a class of threatening diseases which has serious impact on health. Morbidity and mortality rate of malignant tumor is increasing in recent years. Tumorigenesis is a multifactor, multistep, polygene involved process that consists of complex pathological changes, such as activation of a variety of oncogenes, inactivation of tumor suppressor genes, and the disorder of other related regulatory factors. More than 50% of proto-oncogene and oncogene proteins have been characterized with the protein- tyrosine kinase (PTKs) activity. Spleen Tyrosine Kinase (Syk) is a non-receptor type of protein- tyrosine kinase that is widely expressed in hematopoietic cells, lymphocyte, fibroblast and vascular endothelial cells. Syk plays an essential role in lymphocyte development and activation. Recent studies have shown that Syk plays an important role in suppressing the growth and metastasis of human glandular epithelium malignant tumor cells with different origins. However, there was few studies paid attention to the expression of Syk in squamous cell carcinoma. In this study, we investigated the gene and protein expression of Syk in human esophageal squamous cell carcinoma (ESCC) and analyzed the effects of Syk on the biocharacteristics of ESCC.Methods:1 The expression of Syk gene in human esophageal carcinoma tissues (n=30), peri-cancer tissues (n=27) and normal tunica mucosa esophageal tissues (n=30) were detected by Reverse transcription-polymerase chain reaction (RT-PCR) technique. Immunohistochemistry was used to detect the expression of Syk protein in human esophageal carcinoma tissues (n=30), peri-cancer tissues (n=27) and normal tunica mucosa esophageal tissues (n=30). The relationships between the expression of Syk protein and clinical pathology features were analyzed.2 RT-PCR and Western-blot was used to measure the expression of Syk gene and Syk protein in esophageal carcinoma cell lines of Yes-2, Eca-109, TE-13 and TE1 cells.3 Expression of Syk gene was analyzed by RT-PCR, cell migrations were observed by wound healing assay, and expression of MMP-2, MMP-9 was detected by RT-PCR in TE-1 cells after treatment with Piceatannol of different concentrations (0,10,50μmol/L) .4 The methylation status of the 5'CpG island located in the promoter region of Syk gene in esophageal carcinoma cell lines Yes-2 and TE-1 was detected by methylation specific PCR.Results:1 According to the results of RT-PCR, the mRNA expression of the Syk was higher in human esophageal carcinoma lesion tissues than the peri-cancer tissues and the normal esophageal tissues, but among the human esophageal carcinoma lesion tissues, peri-cancer tissues and normal tunica mucosa esophageal tissues the mRNA expression of the Syk had no statistical significance. By immunohistochemical staining with antibody of Sky, it was considered as positive if Syk was expressed in cytoplasm. 34 were Syk protein positive of the human esophageal carcinoma tissues samples (34/39, 87.2%), 18 Syk protein were detected in peri-cancer tissues (18/27, 66.7%) and 26 Syk protein positive of the normal tunica mucosa esophageal tissues (26/38, 68.4%). There was statistical significance among the three groups (P<0.05). The sex, age, tumor size, or pathologic stage of the patients had no influence on the Syk protein (P>0.05).2 By analysis of RT-PCR and Western-blot, Syk mRNA and protein expressed in TE-1,TE-13 and Eca-109 cells, and was strong positive in TE-1 cells,whereas not express in Yes-2 cells.3 Through the detection of RT-PCR method, the expression of Syk gene was gradually decreased after treatment with Piceatannol of different concentrations (0,10,50μmol/L). As the Syk expression decreased, the ability of TE-1 cell migration and invasion was gradually recovered, and MMP-2, MMP-9 were up-regulated after treatment with Piceatannol of different concentrations.4 The results of methylation-specific PCR showed that the promoter of Syk is hypermethylated in Yes-2 cells, while the hypermethylation cannot be detected in TE-1 cell.Conclusions:1 The mRNA and protein expression of Syk in ESCC were significantly higher than peri-cancer tissues and the normal tissues but not associate with the clinical pathology signs.2 The down-regulated expression of Syk might be participate to the migration and invasion in TE-1 cells. The methylation of Syk promoter CpG island might be associated with the gene regulation of squamous cells.
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