Licui Sun1, Jianxin Zhang2, Qiu Yang1, Yang Si3, Yiqun Liu1, Qin Wang1, Feng Han1, Zhenwu Huang4. 1. Department of Nutrition and Metabolism, National Institute for Nutrition and Health, Chinese Center for Disease Control and Prevention, Beijing, P.R. China. 2. Department of Gynecology, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing, P.R. China. 3. Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing, P.R. China. 4. Department of Nutrition and Metabolism, National Institute for Nutrition and Health, Chinese Center for Disease Control and Prevention, Beijing, P.R. China zhenwuhuang@sina.com.
Abstract
BACKGROUND/AIM: To determine the antitumor activities and molecular mechanism of selenium compounds in HeLa cells. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSION: 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. Copyright
BACKGROUND/AIM: To determine the antitumor activities and molecular mechanism of selenium compounds in HeLa cells. MATERIALS AND METHODS: Western blotting was used to detect ERK and AKT activation in HeLa cells induced by selenium compoundsselenomethionine (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. RESULTS: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. CONCLUSION: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. Copyright