S100 calcium binding protein A16 promotes metastasis of gastric cancer
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摘要:
目的：研究S100钙结合蛋白A16（S100 calcium binding protein A16，S100A16）对胃癌细胞迁移的影响及其分子机制。方法：慢病毒感染构建稳定过表达S100A16的胃癌细胞株SGC-7901和MGC-803；划痕实验和Transwell实验检测胃癌细胞的迁移能力；SGC-7901细胞通过脂质体转染S100A16 siRNA，Western blot检测E-钙黏蛋白和波形蛋白；免疫共沉淀检测S100A16和闭合小环蛋白2（zonula occludens 2，ZO-2）的结合情况；免疫荧光观察S100A16和ZO-2在胃癌细胞中的定位。结果：S100A16在胃癌细胞中表达高于胃上皮细胞；稳定过表达S100A16的胃癌细胞SGC-7901和MGC-803构建成功；过表达S100A16促进胃癌细胞SGC-7901和MGC-803迁移；转染S100A16 siRNA抑制SGC-7901细胞中S100A16表达，E-钙黏蛋白表达升高，波形蛋白下调；S100A16和ZO-2存在相互作用，并在空间上存在共定位。结论：S100A16过表达促进胃癌细胞迁移，其作用机制可能是通过和ZO-2相互作用而实现。
Abstract:
Objective：This study aims to investigate the effect and mechanism of S100 calcium binding protein A16 （S100A16） on migration of gastric cancer cells. Methods：Gastric cancer cell lines SGC-7901 and MGC-803 with stable overexpression of S100A16 were constructed by lentivirus infection . Wound healing assay and Transwell assay were used to analyze the migration of gastric cancer cells. Liposome transfection method was used to transfect the S100A16 siRNA into SGC-7901，and expressons of E-Cadherin and Vimentin were detected by Western blot. The interaction between S100A16 and zonula occludens 2（ZO-2） was detected by co-immunoprecipitation. The location of S100A16 and ZO-2 was detected by immunofluorescence. Results：S100A16 expression was higher in gastric cancer cells than in normal gastric epithelial cells. Cell lines with S100A16 overexpression were stably constructed. Overexpression of S100A16 promoted the migration of gastric cancer cells. E-Cadherin protein increased，S100A16 and Vimentin proteins decreased in SGC-7901 cells by transfection of S100A16 siRNA. S100A16 interacted with ZO-2 in SGC-7901 cells. Conclusion：Overexpression of S100A16 promotes the migration of gastric cancer cells. Its mechanism may be through the interaction of ZO-2.
