Silver Nanoparticles Induce HePG-2 Cells Apoptosis Through ROS-Mediated Signaling Pathways
Identifieur interne : 000828 ( Main/Exploration ); précédent : 000827; suivant : 000829Silver Nanoparticles Induce HePG-2 Cells Apoptosis Through ROS-Mediated Signaling Pathways
Auteurs : Bing Zhu ; Yinghua Li ; Zhengfang Lin ; Mingqi Zhao ; Tiantian Xu ; Changbing Wang ; Ning DengSource :
- Nanoscale Research Letters [ 1931-7573 ] ; 2016.
Abstract
Recently, silver nanoparticles (AgNPs) have been shown to provide a novel approach to overcome tumors, especially those of hepatocarcinoma. However, the anticancer mechanism of silver nanoparticles is unclear. Thus, the purpose of this study was to estimate the effect of AgNPs on proliferation and activation of ROS-mediated signaling pathway on human hepatocellular carcinoma HePG-2 cells. A simple chemical method for preparing AgNPs with superior anticancer activity has been showed in this study. AgNPs were detected by transmission electronic microscopy (TEM) and energy dispersive X-ray (EDX). The size distribution and zeta potential of silver nanoparticles were detected by Zetasizer Nano. The average size of AgNPs (2 nm) observably increased the cellular uptake by endocytosis. AgNPs markedly inhibited the proliferation of HePG-2 cells through induction of apoptosis with caspase-3 activation and PARP cleavage. AgNPs with dose-dependent manner significantly increased the apoptotic cell population (sub-G1). Furthermore, AgNP-induced apoptosis was found dependent on the overproduction of reactive oxygen species (ROS) and affecting of MAPKs and AKT signaling and DNA damage-mediated p53 phosphorylation to advance HePG-2 cells apoptosis. Therefore, our results show that the mechanism of ROS-mediated signaling pathways may provide useful information in AgNP-induced HePG-2 cell apoptosis.
Url:
DOI: 10.1186/s11671-016-1419-4
PubMed: 27075340
PubMed Central: 4830774
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Silver Nanoparticles Induce HePG-2 Cells Apoptosis Through ROS-Mediated Signaling Pathways</title><author><name sortKey="Zhu, Bing" sort="Zhu, Bing" uniqKey="Zhu B" first="Bing" last="Zhu">Bing Zhu</name><affiliation><nlm:aff id="Aff1">Guangdong Province Key Laboratory of Molecular Immunology and Antibody Engineering, Jinan University, Guangzhou, Guangdong 510632 People’s Republic of China</nlm:aff><wicri:noCountry code="subfield">Guangdong 510632 People’s Republic of China</wicri:noCountry></affiliation><affiliation><nlm:aff id="Aff2">Virus Laboratory of Guangzhou Women and Children’s Medical Center, Guangzhou, Guangdong 510120 People’s Republic of China</nlm:aff><wicri:noCountry code="subfield">Guangdong 510120 People’s Republic of China</wicri:noCountry></affiliation></author><author><name sortKey="Li, Yinghua" sort="Li, Yinghua" uniqKey="Li Y" first="Yinghua" last="Li">Yinghua Li</name><affiliation><nlm:aff 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People’s Republic of China</wicri:noCountry></affiliation></author><author><name sortKey="Xu, Tiantian" sort="Xu, Tiantian" uniqKey="Xu T" first="Tiantian" last="Xu">Tiantian Xu</name><affiliation><nlm:aff id="Aff2">Virus Laboratory of Guangzhou Women and Children’s Medical Center, Guangzhou, Guangdong 510120 People’s Republic of China</nlm:aff><wicri:noCountry code="subfield">Guangdong 510120 People’s Republic of China</wicri:noCountry></affiliation></author><author><name sortKey="Wang, Changbing" sort="Wang, Changbing" uniqKey="Wang C" first="Changbing" last="Wang">Changbing Wang</name><affiliation><nlm:aff id="Aff2">Virus Laboratory of Guangzhou Women and Children’s Medical Center, Guangzhou, Guangdong 510120 People’s Republic of China</nlm:aff><wicri:noCountry code="subfield">Guangdong 510120 People’s Republic of China</wicri:noCountry></affiliation></author><author><name sortKey="Deng, Ning" sort="Deng, Ning" uniqKey="Deng N" first="Ning" last="Deng">Ning 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code="subfield">Guangdong 510632 People’s Republic of China</wicri:noCountry></affiliation><affiliation><nlm:aff id="Aff2">Virus Laboratory of Guangzhou Women and Children’s Medical Center, Guangzhou, Guangdong 510120 People’s Republic of China</nlm:aff><wicri:noCountry code="subfield">Guangdong 510120 People’s Republic of China</wicri:noCountry></affiliation></author><author><name sortKey="Li, Yinghua" sort="Li, Yinghua" uniqKey="Li Y" first="Yinghua" last="Li">Yinghua Li</name><affiliation><nlm:aff id="Aff2">Virus Laboratory of Guangzhou Women and Children’s Medical Center, Guangzhou, Guangdong 510120 People’s Republic of China</nlm:aff><wicri:noCountry code="subfield">Guangdong 510120 People’s Republic of China</wicri:noCountry></affiliation></author><author><name sortKey="Lin, Zhengfang" sort="Lin, Zhengfang" uniqKey="Lin Z" first="Zhengfang" last="Lin">Zhengfang Lin</name><affiliation><nlm:aff id="Aff2">Virus Laboratory of Guangzhou Women and Children’s Medical Center, Guangzhou, Guangdong 510120 People’s Republic of China</nlm:aff><wicri:noCountry code="subfield">Guangdong 510120 People’s Republic of China</wicri:noCountry></affiliation></author><author><name sortKey="Zhao, Mingqi" sort="Zhao, Mingqi" uniqKey="Zhao M" first="Mingqi" last="Zhao">Mingqi Zhao</name><affiliation><nlm:aff id="Aff2">Virus Laboratory of Guangzhou Women and Children’s Medical Center, Guangzhou, Guangdong 510120 People’s Republic of China</nlm:aff><wicri:noCountry code="subfield">Guangdong 510120 People’s Republic of China</wicri:noCountry></affiliation></author><author><name sortKey="Xu, Tiantian" sort="Xu, Tiantian" uniqKey="Xu T" first="Tiantian" last="Xu">Tiantian Xu</name><affiliation><nlm:aff id="Aff2">Virus Laboratory of Guangzhou Women and Children’s Medical Center, Guangzhou, Guangdong 510120 People’s Republic of China</nlm:aff><wicri:noCountry code="subfield">Guangdong 510120 People’s Republic of China</wicri:noCountry></affiliation></author><author><name sortKey="Wang, Changbing" sort="Wang, Changbing" uniqKey="Wang C" first="Changbing" last="Wang">Changbing Wang</name><affiliation><nlm:aff id="Aff2">Virus Laboratory of Guangzhou Women and Children’s Medical Center, Guangzhou, Guangdong 510120 People’s Republic of China</nlm:aff><wicri:noCountry code="subfield">Guangdong 510120 People’s Republic of China</wicri:noCountry></affiliation></author><author><name sortKey="Deng, Ning" sort="Deng, Ning" uniqKey="Deng N" first="Ning" last="Deng">Ning Deng</name><affiliation><nlm:aff id="Aff1">Guangdong Province Key Laboratory of Molecular Immunology and Antibody Engineering, Jinan University, Guangzhou, Guangdong 510632 People’s Republic of China</nlm:aff><wicri:noCountry code="subfield">Guangdong 510632 People’s Republic of China</wicri:noCountry></affiliation></author></analytic><series><title level="j">Nanoscale Research Letters</title><idno type="ISSN">1931-7573</idno><idno type="eISSN">1556-276X</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Recently, silver nanoparticles (AgNPs) have been shown to provide a novel approach to overcome tumors, especially those of hepatocarcinoma. However, the anticancer mechanism of silver nanoparticles is unclear. Thus, the purpose of this study was to estimate the effect of AgNPs on proliferation and activation of ROS-mediated signaling pathway on human hepatocellular carcinoma HePG-2 cells. A simple chemical method for preparing AgNPs with superior anticancer activity has been showed in this study. AgNPs were detected by transmission electronic microscopy (TEM) and energy dispersive X-ray (EDX). The size distribution and zeta potential of silver nanoparticles were detected by Zetasizer Nano. The average size of AgNPs (2 nm) observably increased the cellular uptake by endocytosis. AgNPs markedly inhibited the proliferation of HePG-2 cells through induction of apoptosis with caspase-3 activation and PARP cleavage. AgNPs with dose-dependent manner significantly increased the apoptotic cell population (sub-G1). Furthermore, AgNP-induced apoptosis was found dependent on the overproduction of reactive oxygen species (ROS) and affecting of MAPKs and AKT signaling and DNA damage-mediated p53 phosphorylation to advance HePG-2 cells apoptosis. Therefore, our results show that the mechanism of ROS-mediated signaling pathways may provide useful information in AgNP-induced HePG-2 cell apoptosis.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Chen, Cl" uniqKey="Chen C">CL Chen</name></author><author><name sortKey="Tseng, Yw" uniqKey="Tseng Y">YW Tseng</name></author><author><name sortKey="Wu, Jc" uniqKey="Wu J">JC Wu</name></author><author><name sortKey="Chen, Gy" uniqKey="Chen G">GY Chen</name></author><author><name sortKey="Lin, Kc" uniqKey="Lin K">KC Lin</name></author><author><name sortKey="Hwang, Sm" uniqKey="Hwang S">SM Hwang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shen, S" uniqKey="Shen S">S Shen</name></author><author><name sortKey="Sun, Cy" uniqKey="Sun C">CY Sun</name></author><author><name sortKey="Du, Xj" uniqKey="Du X">XJ Du</name></author><author><name sortKey="Li, Hj" uniqKey="Li H">HJ 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first="Bing" last="Zhu">Bing Zhu</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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