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© 2017. This work is published under http://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

Lung cancer is the leading cause of male cancer deaths worldwide. Metal-based anticancer drugs have evolved significantly during the past decades. Recently, silver ions have been investigated for their anticancer effects. We aimed to study the time-course cytotoxic effects of silver nitrate on A549 adenocarcinomic human alveolar basal epithelial cells to provide insights into the molecular-level understanding of growth suppression mechanism involved in apoptosis. The influences of silver nitrate were studied via MTT assay, flow cytometry, immunocytochemical, confocal and transmission electron microscopy, and microarray assays. Silver nitrate showed inhibitory effects against A549 cells in a dose- and time-dependent manner for 24, 48, and 72 h and induced apoptosis. The early and late apoptotic cells and depolarized mitochondrial membrane potential were determined by the half-maximal inhibitory concentration (IC50) value of silver nitrate treated for 72 h. But cysteinyl aspartate proteinase-3 was not activated for 72 h. Furthermore, IC50 value of silver nitrate also induced apoptosis according to immunocytochemical assays for 72 h. The downregulated CCNY, HNRNPL, ASF1B, PIAS4, HNRNPH1, EIF2C2, TAF15, FOXC1, LEP, and PCB2 genes administered with silver nitrate IC50 were identified as apoptosis-leading genes. Silver nitrate may be a suitable therapeutic agent against lung cancer.

Details

Title
The apoptotic and genomic studies on A549 cell line induced by silver nitrate
Author
Kaplan, Ayse 1 ; Gulsen Akalin Ciftci 2 ; Kutlu, Hatice Mehtap 1 

 Faculty of Science, Department of Biology, Anadolu University, Eskişehir, Turkey 
 Faculty of Pharmacy, Department of Biochemistry, Anadolu University, Eskişehir, Turkey 
Publication year
2017
Publication date
Apr 2017
Publisher
Sage Publications Ltd.
ISSN
10104283
e-ISSN
14230380
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2113710937
Copyright
© 2017. This work is published under http://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.