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Effects of CS-1 on A431 cell proliferation, cell cycle, and epidermal growth factor receptor signal transduction
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
2012-02-01
DOI10.1093/abbs/gmr111
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
WOS记录号WOS:000299744000005
项目编号20080440288
资助机构Post-doctor Science Foundation of China
引用统计
被引频次:3[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/400002259/59839
专题北京大学药学院_天然药物学系
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
推荐引用方式
GB/T 7714
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.
APA Du, Haiyan.,Xu, Bo.,Wu, Caixia.,Li, Min.,Ran, Fuxiang.,...&Cui, Jingrong.(2012).Effects of CS-1 on A431 cell proliferation, cell cycle, and epidermal growth factor receptor signal transduction.ACTA BIOCHIMICA ET BIOPHYSICA SINICA,44(2),136-146.
MLA Du, Haiyan,et al."Effects of CS-1 on A431 cell proliferation, cell cycle, and epidermal growth factor receptor signal transduction".ACTA BIOCHIMICA ET BIOPHYSICA SINICA 44.2(2012):136-146.
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