论文部分内容阅读
哺乳动物细胞内的某些蛋白质或脂类可以被糖基化修饰,而糖链末端往往存在唾液酸化的现象,催化添加唾液酸的酶为糖基转移酶(sialyltransferase,ST),而去除唾液酸的为唾液酸酶(sialidase,SA或称为neuraminidase,NEU).本实验检测了人膀胱正常上皮细胞HCV29、非浸润性膀胱癌细胞KK47和浸润性膀胱癌细胞YTS-1中唾液酸的表达,发现恶性肿瘤细胞中唾液酸的含量高于正常细胞;进一步分析唾液酸酶和唾液酸转移酶的表达,发现唾液酸酶Neu1在正常细胞中表达最高,在良性肿瘤细胞中次之,在恶性肿瘤细胞中表达最低,推测在膀胱癌中Neu1对唾液酸的异常表达起着主要作用.同时,膀胱癌细胞中Toll样受体1,2,3,4(toll-like receptors,TLRs)表达趋势也与Neu1一致.利用TGF-β处理HCV29,使之发生上皮间质转化(epithelial-mesenchymal transition,EMT),细胞中Neu1和TLR3表达明显减少;将Neu1基因沉默后,TLR3表达也明显减少.此外,在YTS-1细胞中过表达Neu1,TLR3表达增高且激活了下游NF-κB通路.这一结果说明膀胱癌中Neu1与TLR3的表达有着密切的关系,这为膀胱癌的分子机理研究提供了工作基础.
Certain proteins or lipids in mammalian cells may be glycosylated, while sialylation often occurs at the ends of the sugar chain. The enzyme that catalyzes the addition of sialic acid is sialyltransferase (ST), whereas sialic acid Sialidase (SA) or neuraminidase (NEU) .We tested the expression of sialic acid in human normal bladder epithelial cells HCV29, non-invasive bladder cancer cells KK47 and invasive bladder cancer cells YTS-1, Found that the content of sialic acid in malignant tumor cells was higher than normal cells. Further analysis of the expression of sialidase and sialyltransferase showed that sialidase Neu1 was the highest expression in normal cells, followed by benign tumor cells, The expression of sialic acid in Neu1 bladder cancer cells is the lowest, suggesting that Neu1 plays an important role in the abnormal expression of sialic acid in bladder cancer cells.At the same time, the tendency of Toll-like receptors 1, 2, 3 and 4 (toll-like receptors, TLRs) Which was consistent with that of Neu1. The expression of Neu1 and TLR3 was significantly decreased in epithelial-mesenchymal transition (EMT) cells treated with TGF-β, and the expression of TLR3 was significantly decreased after Neu1 gene silencing .In addition, overexpression of Neu1 in YTS-1 cells resulted in increased expression of TLR3 and activation of downstream NF-κB pathway.This result indicates that there is a close relationship between Neu1 and TLR3 expression in bladder cancer, which is the molecular mechanism of bladder cancer Provided a working basis.