Study On Mechanism Of SIDT2and Gastric Tumorigenesis

Objective:To explore SIDT2expression level in gastric cancer tissues and cancer cell lines as well as the downstream target genes modulated by SIDT2. Simultaneously a further comprehension of the STDT2expression involved in the mechanism of gastric carcinogenesis may be investigated.Methods:Cancer and paracancerous specimens were obtained from40patients who received gastrectomy and have complete clinical data. RNAi, qPCR, Western Blot, cell culture, bioinformatics technology were used in the experiment to detect the expression level of SIDT2as well as the relationship between the clinical features and SIDT2expression.Meanwhile RNAi was used to silence the expression of SIDT2in gastric cancer cell lines to observe the effect which applied to the downstream gene expression profile. Annotation and classification on the screened gene group was carried out according to the biological pathways, molecular function and cellular localization.Results:①Expression of SIDT2mRNA in gastric cancer tissues was1.9519±0.21times of that in paracancerous tissues, and the difference was statistically significant (P=0.000).SIDT2mRNA expression level in gastric cancer was associated with the degree of differentiation, SIDT2mRNA expression level in low differentiation group was higher than that of high differentiation group (P=0.000)。②Expression of SIDT2protein in gastric cancer was significantly higher than that in paracancerous tissue(P=0.020). SIDT2protein expression in gastric paracancerous tissues was correlated with the degree of differentiation, undifferentiated group was significantly higher than that in high differentiation group(P=0.025).Compared with the control group, the expression profile of SIDT2silenced by SIDT2-siRNA in SGC-7901cells was changed:46genes were affected, including1up-regulated,45genes down-regulated. There exists a repeat for times of PDCD6and TMBIM6, HISTIH2AC and HISTIH2BH, and so on in the KEGG, GenMAPP and Biocarta databases.Conclusions:There exists abnormal overexpression of SIDT2in gastric cancer, and the expression of SIDT2may influence cell differentiation involving in gastric tumorigenesis. The downstream gene expression profile was changed as silenced SIDT2expression. PDCD6may correlate with TMBIM in function, and SIDT2probably involved in the occurrence and development of gastric cancer by affecting PDCD6and other factors, thus further study is needed.