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学科主题: 药学
题名:
Vanadyl bisacetylacetonate induced G1/S cell cycle arrest via high-intensity ERK phosphorylation in HepG2 cells
作者: 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
发表日期: 2008-08-01
DOI: 10.1007/s00775-008-0387-2
卷: 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
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/55692
Appears in Collections:北京大学药学院_化学生物学系_期刊论文

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作者单位: Peking Univ, Hlth Sci Ctr, Sch Pharmaceut Sci, Dept Biol Chem, Beijing 100083, Peoples R China

Recommended Citation:
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.
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