Tetrazolium Violet Induced Apoptosis and Cell Cycle Arrest in Human Lung Cancer A549 Cells
文献类型：期刊论文
| 作者 | Zhang, Xiao-Hong1,2; Zhang, Nan3; Lu, Jian-Mei4; Kong, Qing-Zhong1; Zhao, Yun-Feng1,2 |
| 刊名 | biomolecules & therapeutics
 |
| 出版日期 | 2012-03-31 |
| 卷号 | 20期号:2页码:177-182 |
| 关键词 | A549 cell apoptosis Fas Fas ligand p21 p53 Tetrazolium violet |
| ISSN号 | 1976-9148 |
| 中文摘要 | tetrazolium violet is a tetrazolium salt and has been proposed as an antitumor agent. in this study, we reported for the first time that tetrazolium violet not only inhibited human lung cancer a549 cell proliferation but also induced apoptosis and blocked cell cycle progression in the g1 phase. the results showed that tetrazolium violet significantly decreased the viability of a549 cells at 5-15 mu m. tetrazolium violet -induced apoptosis in a549 cells was confirmed by h33258 staining assay. in a549, tetrazolium violet blocked the progression of the cell cycle at g1 phase by inducing p53 expression and further up-regulating p21/waf1 expression. in addition, an enhancement in fas/apo-1 and its two forms of ligands, membrane-bound fas ligand (mfasl) and soluble fas ligand (sfasl), as well as caspase, were responsible for the apoptotic effect induced by tetrazolium violet. the conclusion of this study is that tetrazolium violet induced p53 expression which caused cell cycle arrest and apoptosis. these findings suggest that tetrazolium violet has strong potential for development as an agent for treatment lung cancer. |
| 英文摘要 | tetrazolium violet is a tetrazolium salt and has been proposed as an antitumor agent. in this study, we reported for the first time that tetrazolium violet not only inhibited human lung cancer a549 cell proliferation but also induced apoptosis and blocked cell cycle progression in the g1 phase. the results showed that tetrazolium violet significantly decreased the viability of a549 cells at 5-15 mu m. tetrazolium violet -induced apoptosis in a549 cells was confirmed by h33258 staining assay. in a549, tetrazolium violet blocked the progression of the cell cycle at g1 phase by inducing p53 expression and further up-regulating p21/waf1 expression. in addition, an enhancement in fas/apo-1 and its two forms of ligands, membrane-bound fas ligand (mfasl) and soluble fas ligand (sfasl), as well as caspase, were responsible for the apoptotic effect induced by tetrazolium violet. the conclusion of this study is that tetrazolium violet induced p53 expression which caused cell cycle arrest and apoptosis. these findings suggest that tetrazolium violet has strong potential for development as an agent for treatment lung cancer. |
| WOS标题词 | science & technology ; life sciences & biomedicine |
| 类目[WOS] | biochemistry & molecular biology ; pharmacology & pharmacy |
| 研究领域[WOS] | biochemistry & molecular biology ; pharmacology & pharmacy |
| 关键词[WOS] | up-regulation ; mediated apoptosis ; caspase activation ; tumor-cells ; hepg2 cells ; fas ; p53 ; death ; pathways ; protein |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000303224300007 |
| 公开日期 | 2013-03-15 |
| 源URL | [http://ir.nwipb.ac.cn/handle/363003/3704]  |
| 专题 | 西北高原生物研究所_中国科学院西北高原生物研究所 |
| 作者单位 | 1.Shandong Univ, Sch Life Sci, Jinan 250100, Peoples R China 2.Chinese Acad Sci, NW Inst Plateau Biol, Xining 810008, Peoples R China 3.Jinan Cent Hosp, Dept Med, Jinan, Shandong Provin, Peoples R China 4.Qufu Normal Univ, Sch Life Sci, Qufu 273165, Peoples R China |
| 推荐引用方式 GB/T 7714 | Zhang, Xiao-Hong,Zhang, Nan,Lu, Jian-Mei,et al. Tetrazolium Violet Induced Apoptosis and Cell Cycle Arrest in Human Lung Cancer A549 Cells[J]. biomolecules & therapeutics,2012,20(2):177-182. |
| APA | Zhang, Xiao-Hong,Zhang, Nan,Lu, Jian-Mei,Kong, Qing-Zhong,&Zhao, Yun-Feng.(2012).Tetrazolium Violet Induced Apoptosis and Cell Cycle Arrest in Human Lung Cancer A549 Cells.biomolecules & therapeutics,20(2),177-182. |
| MLA | Zhang, Xiao-Hong,et al."Tetrazolium Violet Induced Apoptosis and Cell Cycle Arrest in Human Lung Cancer A549 Cells".biomolecules & therapeutics 20.2(2012):177-182. |
入库方式： OAI收割
来源：西北高原生物研究所
浏览0
下载0
收藏0
其他版本
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。