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Vanadium compounds discriminate hepatoma and normal hepatic cells by differential regulation of reactive oxygen species
Wang, Qin1,2; Liu, Tong-Tong1,2; Fu, Ying1; Wang, Kui1,2; Yang, Xiao-Gai1
关键词Vanadium compounds Reactive oxygen species Antioxidant Cell cycle arrest
刊名JOURNAL OF BIOLOGICAL INORGANIC CHEMISTRY
2010-09-01
DOI10.1007/s00775-010-0668-4
15期:7页:1087-1097
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Chemistry, Inorganic & Nuclear
研究领域[WOS]Biochemistry & Molecular Biology ; Chemistry
关键词[WOS]ACTIVATED PROTEIN-KINASE ; HEPATOCELLULAR-CARCINOMA ; OXIDATIVE STRESS ; CANCER-TREATMENT ; TUMOR-CELLS ; VANADATE ; PATHWAY ; APOPTOSIS ; EXPRESSION ; INDUCTION
英文摘要

Our previous study indicated that vanadium compounds can block cell cycle progression at the G1/S phase in human hepatoma HepG2 cells via a highly activated extracellular signal-regulated protein kinase (ERK) signal. To explore their differential action on normal cells, we investigated the response of an immortalized hepatic cell line, L02 cells. The results demonstrated that a higher concentration of vanadium compounds was needed to inhibit L02 proliferation, which was associated with S and G2/M cell cycle arrest. In addition, in contrast to insignificant reactive oxygen species (ROS) generation in HepG2 cells, all of the vanadium compounds resulted significant increases in both O (2) (center dot-) and H(2)O(2) levels in L02 cells. At the same time, ERK and c-Jun N-terminal kinase (JNK) as well as cell division control protein 2 homolog (Cdc2) were found to be highly phosphorylated, which could be counteracted with the antioxidant N-acetylcysteine (NAC). The current study also demonstrated that both the ERK and the JNK pathways contributed to the cell cycle arrest induced by vanadium compounds in L02 cells. More importantly, it was found that although NAC can ameliorate the cytotoxicity of vanadium compounds in L02 cells, it did not decrease their cytotoxicity in HepG2 cells. It thus shed light on the potential therapeutic applications of vanadium compounds with antioxidants as synergistic agents to reduce their toxicities in human normal cells without affecting their antitumor activities in cancer cells.

语种英语
WOS记录号WOS:000281597900010
项目编号20871008
资助机构National Natural Science Foundation of China ; Scientific Research Foundation for Returned Overseas Chinese Scholars, State Education Ministry
引用统计
被引频次:31[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/66327
专题北京大学药学院_化学生物学系
北京大学第三临床医学院_超声影像科
作者单位1.Peking Univ, Dept Biol Chem, Sch Pharmaceut Sci, Beijing 100191, Peoples R China
2.Peking Univ, State Key Lab Nat & Biomimet Drugs, Sch Pharmaceut Sci, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Wang, Qin,Liu, Tong-Tong,Fu, Ying,et al. Vanadium compounds discriminate hepatoma and normal hepatic cells by differential regulation of reactive oxygen species[J]. JOURNAL OF BIOLOGICAL INORGANIC CHEMISTRY,2010,15(7):1087-1097.
APA Wang, Qin,Liu, Tong-Tong,Fu, Ying,Wang, Kui,&Yang, Xiao-Gai.(2010).Vanadium compounds discriminate hepatoma and normal hepatic cells by differential regulation of reactive oxygen species.JOURNAL OF BIOLOGICAL INORGANIC CHEMISTRY,15(7),1087-1097.
MLA Wang, Qin,et al."Vanadium compounds discriminate hepatoma and normal hepatic cells by differential regulation of reactive oxygen species".JOURNAL OF BIOLOGICAL INORGANIC CHEMISTRY 15.7(2010):1087-1097.
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