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Turning On/Off the Anti-Tumor Effect of the Au Cluster via Atomically Controlling Its Molecular Size
Zhai, Jiao2,3; Jia, Yanwei2; Zhao, Lina3; Yuan, Cling1,3; Gao, Fuping3; Zhang, Xiangchun3; Cai, Pengju3; Gan, Liang1; Guo, Juanjuan3; Yi, Shuhong4; Chai, Zhifang3; Zhao, Yuliang3; Gao, Xueyun1,3
2018-05
Source PublicationACS NANO
ISSN1936-0851
Volume12Issue:5Pages:4378-4386
Abstract

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.

KeywordPeptide-au Cluster Antitumor Effect Mitochondria Puma Mcl-1 Cell Apoptosis
DOI10.1021/acsnano.8b00027
URLView the original
Indexed BySCI
Language英语
WOS Research AreaChemistry ; Science & Technology - Other Topics ; Materials Science
WOS SubjectChemistry, Multidisciplinary ; Chemistry, Physical ; Nanoscience & Nanotechnology ; Materials Science, Multidisciplinary
WOS IDWOS:000433404500033
PublisherAMER CHEMICAL SOC
The Source to ArticleWOS
Fulltext Access
Citation statistics
Cited Times [WOS]:6   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionINSTITUTE OF MICROELECTRONICS
Corresponding AuthorGao, Xueyun
Affiliation1.Department of Chemistry and Chemical Engineering, Beijing University of Technology, Beijing 100124, China
2.State Key Laboratory of Analog and Mixed Signal VLSI, University of Macau, Macao, SAR, China
3.CAS Key Laboratory for Biological Effects of Nanomaterials and Nanosafety, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing 100049, China
4.Liver Transplantation Center, the Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510000, China
First Author AffilicationUniversity of Macau
Recommended Citation
GB/T 7714
Zhai, Jiao,Jia, Yanwei,Zhao, Lina,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 Zhai, Jiao.,Jia, Yanwei.,Zhao, Lina.,Yuan, Cling.,Gao, Fuping.,...&Gao, Xueyun.(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 Zhai, Jiao,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.
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