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学科主题: 药学
题名:
Effects of CS-1 on A431 cell proliferation, cell cycle, and epidermal growth factor receptor signal transduction
作者: Du, Haiyan1,2; Xu, Bo1; Wu, Caixia3; Li, Min1; Ran, Fuxiang1; Cai, Shaoqing4; Cui, Jingrong1
关键词: CS-1 ; cell cycle ; EGFR signaling pathway ; high content screening
刊名: ACTA BIOCHIMICA ET BIOPHYSICA SINICA
发表日期: 2012-02-01
DOI: 10.1093/abbs/gmr111
卷: 44, 期:2, 页:136-146
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology ; Biophysics
研究领域[WOS]: Biochemistry & Molecular Biology ; Biophysics
关键词[WOS]: NASOPHARYNGEAL CARCINOMA-CELLS ; KINASE ; INHIBITION ; ACTIVATION ; EXPRESSION
英文摘要:

CS-1, a new alkaloid with a molecular formula of C21H20O8N2S, is extracted from traditional Chinese medicine. Previous studies have shown that CS-1 can inhibit the proliferation of several human carcinoma cells in vivo and in vitro. The aims of this study are to investigate the anti-tumor effect and mechanism of CS-1 in epidermal growth factor receptor (EGFR) signaling pathway in human A431 cell line. Through the sulforhodamine B assay, we found that CS-1 inhibited A431 cell proliferation in the concentration- and time-dependent manners. The inhibitory rate ranged from 14.5% to 87.8% after 24 h of incubation. High content screening (HCS) multi-parameters cytotoxicity analysis showed that CS-1 at high concentration had slight cytotoxicity that resulted from the cell permeabilization and slight reduction in total mitochondrial mass, whereas no change in nucleus size/morphology and lysosomal mass-pH was found. The cytotoxicity of CS-1 was not a major reason for its anti-proliferative effect. Cell cycle analysis indicated that CS-1 induced G1-phase arrest in A431 cells in a time-dependent manner at high concentration (2.5 mu M), and S-phase arrest at low concentration (0.625 mu M). The HCS assay also showed that CS-1 could inhibit the EGFR internalization, extracellular-signal-regulated kinase (Erk)/mitogen-activated protein kinase translocation to nucleus, the accumulation of phosphorylated protein kinase B (Akt), signal transducer and activator of transcription 3 (STAT3), and cyclin D1 in the nucleus. These results were confirmed by the western blot analysis. CS-1 might inhibit the epidermal growth factor binding to its receptor, resulting in the inhibition of the accumulation of phosphorylated Erk and Akt, and STAT3 in the nucleus, and affecting the transcription of cyclin D1 and cell cycle arrest in G1/S phase.

语种: 英语
所属项目编号: 20080440288
项目资助者: Post-doctor Science Foundation of China
WOS记录号: WOS:000299744000005
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/59839
Appears in Collections:北京大学药学院_天然药物学系_期刊论文

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作者单位: 1.Shandong Med Coll, Linyi 276000, Peoples R China
2.Peking Univ, State Key Lab Nat & Biomimet Drugs, Beijing 100191, Peoples R China
3.Capital Med Univ, Drug Clin Trail Inst, Beijing Anzhen Hosp, Beijing 100029, Peoples R China
4.Peking Univ, Dept Nat Med, Sch Pharmaceut Sci, Beijing 100191, Peoples R China

Recommended Citation:
Du, Haiyan,Xu, Bo,Wu, Caixia,et al. Effects of CS-1 on A431 cell proliferation, cell cycle, and epidermal growth factor receptor signal transduction[J]. ACTA BIOCHIMICA ET BIOPHYSICA SINICA,2012,44(2):136-146.
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