Sun Licui, Zhang Jianxin, Yang Qiu, Si Yang, Liu Yiqun, Wang Qin, Han Feng, Huang Zhenwu
Department of Nutrition and Metabolism, National Institute for Nutrition and Health, Chinese Center for Disease Control and Prevention, Beijing, P.R. China.
Department of Gynecology, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing, P.R. China.
Anticancer Res. 2017 Aug;37(8):4433-4441. doi: 10.21873/anticanres.11838.
BACKGROUND/AIM: To determine the antitumor activities and molecular mechanism of selenium compounds in HeLa cells.
Western blotting was used to detect ERK and AKT activation in HeLa cells induced by selenium compounds selenomethionine (SeMet), methylselenocysteine (MeSeCys) and methylseleninic acids (MeSeA). Using MTT, wound-healing and Matrigel adhesion assays, the antitumor effects of SAM and selenium compounds were evaluated in HeLa cells.
MeSeA inhibited ERK and AKT signaling pathways and suppressed the proliferation (p<0.05 vs. HeLa control), migration (p<0.05 vs. HeLa control) and adhesion (p<0.01 vs. HeLa control) of HeLa cells. MeSeCys and SeMet inhibited AKT signaling pathways and the migration (p<0.05 vs. HeLa control) and adhesion (p<0.01 vs. HeLa control) of HeLa cells. The synergistic action of MeSeA with SAM led to a statistically significant inhibition of proliferation, migration and adhesion of HeLa cells.
MeSeA, MeSeCys and SeMet exert different antitumor activities by inhibiting ERK and AKT signaling pathways. The combination of MeSeA and SAM exhibited better antitumor effects compared to the other treatments.
背景/目的：确定硒化合物对人宫颈癌HeLa细胞的抗肿瘤活性及分子机制。
采用蛋白质免疫印迹法检测硒化合物硒代蛋氨酸（SeMet）、甲基硒代半胱氨酸（MeSeCys）和甲基亚硒酸（MeSeA）诱导的HeLa细胞中ERK和AKT的激活情况。利用MTT法、划痕愈合实验和基质胶黏附实验评估SAM和硒化合物对HeLa细胞的抗肿瘤作用。
MeSeA抑制ERK和AKT信号通路，并抑制HeLa细胞的增殖（与HeLa对照组相比，p<0.05）、迁移（与HeLa对照组相比，p<0.05）和黏附（与HeLa对照组相比，p<0.01）。MeSeCys和SeMet抑制AKT信号通路以及HeLa细胞的迁移（与HeLa对照组相比，p<0.05）和黏附（与HeLa对照组相比，p<0.01）。MeSeA与SAM的协同作用导致HeLa细胞的增殖、迁移和黏附受到统计学上显著的抑制。
MeSeA、MeSeCys和SeMet通过抑制ERK和AKT信号通路发挥不同的抗肿瘤活性。与其他处理相比，MeSeA和SAM联合使用表现出更好的抗肿瘤效果。
