IR@PKUHSC  > 北京大学药学院  > 化学生物学系
学科主题药学
Vanadyl bisacetylacetonate induced G1/S cell cycle arrest via high-intensity ERK phosphorylation in HepG2 cells
Fu, Ying; Wang, Qin; Yang, Xiao-Gai; Yang, Xiao-Da; Wang, Kui
关键词Hepg2 Vanadyl Bisacetylacetonate Cell Cycle Arrest Extracellular Signal-regulated Protein Kinase Retinoblastoma Tumor Suppressor Protein
刊名JOURNAL OF BIOLOGICAL INORGANIC CHEMISTRY
2008-08-01
DOI10.1007/s00775-008-0387-2
13期:6页:1001-1009
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]OXIDATIVE DNA-DAMAGE ; CHANG LIVER-CELLS ; CANCER-TREATMENT ; PHASE ARREST ; C141 CELLS ; ACTIVATION ; GROWTH ; COMPLEXES ; PATHWAY ; PROTEIN
英文摘要

In recent years the anticancer properties of vanadium compounds have been noticed, but the underlying mechanisms are not well understood. In the present work, we found that vanadyl bisacetylacetonate ([VO(acac)(2)]) blocked cell cycle progression permanently at G1 phase in a dose- and time-dependent manner in HepG2 cells. This was further evidenced by the growth regulatory signals during the G1 stage. After the treatment with [VO(acac)(2)], the level of phophorylation of retinoblastoma tumor suppressor protein (pRb) and the expressions of cyclin D1, cyclin E and cyclin A were reduced, while the expression of a cyclin-dependent kinase inhibitor p21 was increased dose-dependently. In the meantime, neither O(2)(center dot-) nor H(2)O(2) level was observed to increase. Interestingly, the levels of phosphorylated extracellular signal-regulated protein kinase (ERK) and Akt were highly activated. After 1-h pretreatment with a lower concentration of MEK inhibitor U0126, the level of phosphorylated pRb was restored, indicating a release of cell cycle arrest. Taken together, we suggested that [VO(acac)(2)]-induced proliferation inhibition was caused by G1/S cell cycle arrest, which resulted from the decreased level of phosphorylated pRb in its active hypophosphorylated form via a highly activated ERK signal in HepG2 cells. The results presented here provided new insight into the development of vanadium compounds as potential anticancer agents.

语种英语
WOS记录号WOS:000257934500015
引用统计
被引频次:39[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/400002259/55692
专题北京大学药学院_化学生物学系
作者单位Peking Univ, Hlth Sci Ctr, Sch Pharmaceut Sci, Dept Biol Chem, Beijing 100083, Peoples R China
推荐引用方式
GB/T 7714
Fu, Ying,Wang, Qin,Yang, Xiao-Gai,et al. Vanadyl bisacetylacetonate induced G1/S cell cycle arrest via high-intensity ERK phosphorylation in HepG2 cells[J]. JOURNAL OF BIOLOGICAL INORGANIC CHEMISTRY,2008,13(6):1001-1009.
APA Fu, Ying,Wang, Qin,Yang, Xiao-Gai,Yang, Xiao-Da,&Wang, Kui.(2008).Vanadyl bisacetylacetonate induced G1/S cell cycle arrest via high-intensity ERK phosphorylation in HepG2 cells.JOURNAL OF BIOLOGICAL INORGANIC CHEMISTRY,13(6),1001-1009.
MLA Fu, Ying,et al."Vanadyl bisacetylacetonate induced G1/S cell cycle arrest via high-intensity ERK phosphorylation in HepG2 cells".JOURNAL OF BIOLOGICAL INORGANIC CHEMISTRY 13.6(2008):1001-1009.
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Fu, Ying]的文章
[Wang, Qin]的文章
[Yang, Xiao-Gai]的文章
百度学术
百度学术中相似的文章
[Fu, Ying]的文章
[Wang, Qin]的文章
[Yang, Xiao-Gai]的文章
必应学术
必应学术中相似的文章
[Fu, Ying]的文章
[Wang, Qin]的文章
[Yang, Xiao-Gai]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。