过表达α1,3-岩藻糖基转移酶Ⅶ通过增强p38MAPK信号通路抑制UVC照射诱导的人肝癌SMMC-7721细胞的凋亡

 目的 初步探讨α1,3-岩藻糖基转移酶Ⅶ（简称FUT7）在UVC照射诱导的人肝癌SMMC-7721(简称7721)细胞凋亡过程中的作用及机制。方法 用RT-PCR检测转染pcDNA3-FUT7质粒的7721细胞及转染空质粒pcDNA3的7721细胞中FUT7基因的转录水平；用流式细胞仪检测细胞表面FUT7产物SLex的表达水平；利用DAPI染核计算UVC照射后细胞的凋亡比率；用结晶紫染色法测定细胞的存活率；利用Western blot检测Caspase3的剪切情况及p38MAPK、JNK1/2和ERK1/2的磷酸化水平。结果 过表达FUT7能抑制UVC照射诱导的7721细胞凋亡，同时还增强了细胞中p38MAPK信号通路的活性，而用p38MAPK的特异性抑制剂处理则可削弱FUT7的抗凋亡作用。结论 在UVC照射诱导的7721细胞凋亡过程中FUT7具有抗凋亡的作用，这种作用可能部分通过增强p38MAPK信号通路活性而实现。

Overexpression of α1,3-fucosyltransferaseⅦ attenuates UVC-induced apoptosis of SMMC-7721 cells through enhancing p38MAPK-signaling pathway

Objective To study the role of α1, 3-fucosyltransferaseVII(FUT7) in UVC-induced apoptosis of human hepatocarcinoma cell line SMMC-7721 (7721). Methods The expression of FUT7 in both pcDNA3-FUT7 transfectant and mock pcDNA3 transfectant cells were detected by RT-PCR. The level of SLex was detected by flow cytometry. Apoptotic percentage was detected by DAPI staining. Survival percentage was detected by crystal violet staining. The levels of cleaved caspase3 and phosphorylation of p38MAPK, JNK1/2 and ERK1/2 were detected by western blot. Results Overexpression of FUT7 attenuated UVC-induced apoptosis of 7721 and enhanced p38MAPK-signaling pathway. In addition, pretreatment with specific p38MAPK inhibitor reduced the anti-apoptotic effect of FUT7. Conclusions FUT7 functions as an anti-apoptotic molecule during UVC-induced apoptosis, at least in part, through enhancing p38MAPK-signaling pathway.