Turning On/Off the Anti-Tumor Effect of the Au Cluster via Atomically Controlling Its Molecular Size
文献类型：期刊论文
| 作者 | Guo JJ(郭娟娟) ; Chai ZF(柴之芳); Zhao YL(赵宇亮); Gao XY(高学云); Zhai, J; Jia, YW; Zhao, LN; Yuan, C; Gao, FP; Zhang, XC
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| 刊名 | ACS NANO
 |
| 出版日期 | 2018 |
| 卷号 | 12期号:5页码:4378-4386 |
| ISSN号 | 1936-0851 |
| 关键词 | peptide-Au cluster antitumor effect mitochondria Puma Mcl-1 cell apoptosis |
| DOI | 10.1021/acsnano.8b00027 |
| 文献子类 | Article |
| 英文摘要 | We reported two Au clusters with precisely controlled molecular size (Au(5)Peptide(3) and Au(22)Peptide(10)) showing different antitumor effects. In vitro, both Au(5)Peptide(3) and Au(22)Peptide(10) were well taken up by human nasopharyngeal cancer cells (CNE1 cells). However, only Au(5)Peptide(3) significantly induced CNE1 cell apoptosis. Further studies showed that CNE1 cells took up Au(5)Peptide(3) (1.98 X 10(-15) mol/cell), and 9% of them entered mitochondria (0.186 X 10(-15) mol/cell). As a comparison, the uptake of Au(22)peptide(10) was only half the amount of Au(5)Peptide(3) (1.11 X 10(-15) mol/cell), and only 1% of them entered mitochondria (0.016 X 10(-15) mol/cell). That gave 11.6-fold more Au(5)Peptide(3) in mitochondria of CNE1 cells than Au(22)Peptide(10). Further cell studies revealed that the antitumor effect may be due to the enrichment of Au(5)Peptide(3) in mitochondria. Au(5)Peptide(3) slightly decreased the Mcl-1 (antiapoptotic protein of mitochondria) and significantly increased the Puma (pro-apoptotic protein of mitochondria) expression level in CNE1 cells, which resulted in mitochondrial transmembrane potential change and triggered the caspase 9 caspase 3 PARP pathway to induce CNE1 cell apoptosis. In vivo, CNE1 tumor growth was significantly suppressed by Au(5)Peptide(3) in the xenograft model after 3 weeks of intraperitoneal injection. The TUNEL and immuno-histochemical studies of tumor tissue verified that CNE1 cell apoptosis was mainly via the Puma and Mcl-1 apoptosis pathway in the xenograft model, which matched the aforementioned CNE1 cell studies in vitro. The discovery of Au-5 but not Au-22 suppressing tumor growth via the mitochondria target was a breakthrough in the nanomedical field, as this provided a robust approach to turn on/off the nanoparticles' medical properties via atomically controlling their sizes. |
| 电子版国际标准刊号 | 1936-086X |
| WOS关键词 | GROWTH-FACTOR RECEPTOR ; CANCER-CELLS ; METAL NANOCLUSTERS ; GOLD NANOCLUSTERS ; APOPTOSIS ; PROTEIN ; PEPTIDE ; DEATH ; PUMA |
| WOS研究方向 | Chemistry ; Science & Technology - Other Topics ; Materials Science |
| 语种 | 英语 |
| WOS记录号 | WOS:000433404500033 |
| 源URL | [http://ir.ihep.ac.cn/handle/311005/285961]  |
| 专题 | 高能物理研究所_多学科研究中心 |
| 通讯作者 | Gao XY(高学云) |
| 作者单位 | 中国科学院高能物理研究所 |
| 推荐引用方式 GB/T 7714 | Guo JJ,Chai ZF,Zhao YL,et al. Turning On/Off the Anti-Tumor Effect of the Au Cluster via Atomically Controlling Its Molecular Size[J]. ACS NANO,2018,12(5):4378-4386. |
| APA | 郭娟娟.,柴之芳.,赵宇亮.,高学云.,Zhai, J.,...&蔡鹏举.(2018).Turning On/Off the Anti-Tumor Effect of the Au Cluster via Atomically Controlling Its Molecular Size.ACS NANO,12(5),4378-4386. |
| MLA | 郭娟娟,et al."Turning On/Off the Anti-Tumor Effect of the Au Cluster via Atomically Controlling Its Molecular Size".ACS NANO 12.5(2018):4378-4386. |
入库方式： OAI收割
来源：高能物理研究所
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