Silver nanoparticles inhibit the function of hypoxia-inducible factor-1 and target genes: insight into the cytotoxicity and antiangiogenesis.
- Publisher:
- DOVE MEDICAL PRESS LTD
- Publication Type:
- Journal Article
- Citation:
- Int J Nanomedicine, 2016, 11, pp. 6679-6692
- Issue Date:
- 2016
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author |
Yang, T https://orcid.org/0000-0002-8683-2072 |
|
dc.contributor.author | Yao, Q | |
dc.contributor.author | Cao, F | |
dc.contributor.author | Liu, Q | |
dc.contributor.author | Liu, B | |
dc.contributor.author | Wang, X-H | |
dc.date.accessioned | 2022-08-15T21:49:29Z | |
dc.date.available | 2022-08-15T21:49:29Z | |
dc.date.issued | 2016 | |
dc.identifier.citation | Int J Nanomedicine, 2016, 11, pp. 6679-6692 | |
dc.identifier.issn | 1176-9114 | |
dc.identifier.issn | 1178-2013 | |
dc.identifier.uri | http://hdl.handle.net/10453/160262 | |
dc.description.abstract | Hypoxia-inducible factor-1 (HIF-1) is a transcription factor that is activated upon exposure to hypoxic stress. It modulates a number of cellular responses including proliferation, apoptosis, angiogenesis, and metabolism by activating a panel of target genes in response to hypoxia. The HIF-1 level is often upregulated in the hypoxic microenvironment of solid tumors, which contributes to cancer treatment failure. Here we report that silver nanoparticles (AgNPs), which are widely used as an antimicrobial agent, are an effective inhibitor of HIF-1. AgNPs inhibited the activation of a HIF-dependent reporter construct after the cells were exposed to hypoxic conditions or treated with cobalt chloride, a hypoxia mimetic agent. The AgNPs also interfered with the accumulation of HIF-1α protein and the induction of the endogenous HIF target genes, VEGF-A and GLUT1. Since both HIF-1 and vascular endothelial growth factor-A play an important role in angiogenesis, AgNPs also inhibited angiogenesis in vitro. Our data reveal a new mechanism of how AgNPs act on cellular function, that is, they disrupt HIF signaling pathway. This finding provides a novel insight into how AgNPs can inhibit cancer cell growth and angiogenesis. | |
dc.format | Electronic-eCollection | |
dc.language | eng | |
dc.publisher | DOVE MEDICAL PRESS LTD | |
dc.relation.ispartof | Int J Nanomedicine | |
dc.relation.isbasedon | 10.2147/IJN.S109695 | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | 0601 Biochemistry and Cell Biology, 1007 Nanotechnology, 1115 Pharmacology and Pharmaceutical Sciences | |
dc.subject.classification | Nanoscience & Nanotechnology | |
dc.subject.mesh | Apoptosis | |
dc.subject.mesh | Blotting, Western | |
dc.subject.mesh | Cell Proliferation | |
dc.subject.mesh | Glucose Transporter Type 1 | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Hypoxia | |
dc.subject.mesh | Hypoxia-Inducible Factor 1, alpha Subunit | |
dc.subject.mesh | Nanoparticles | |
dc.subject.mesh | Neoplasms | |
dc.subject.mesh | Neovascularization, Pathologic | |
dc.subject.mesh | RNA, Messenger | |
dc.subject.mesh | Real-Time Polymerase Chain Reaction | |
dc.subject.mesh | Reverse Transcriptase Polymerase Chain Reaction | |
dc.subject.mesh | Signal Transduction | |
dc.subject.mesh | Silver | |
dc.subject.mesh | Tumor Cells, Cultured | |
dc.subject.mesh | Vascular Endothelial Growth Factor A | |
dc.subject.mesh | Tumor Cells, Cultured | |
dc.subject.mesh | Humans | |
dc.subject.mesh | Neoplasms | |
dc.subject.mesh | Neovascularization, Pathologic | |
dc.subject.mesh | Silver | |
dc.subject.mesh | Vascular Endothelial Growth Factor A | |
dc.subject.mesh | RNA, Messenger | |
dc.subject.mesh | Blotting, Western | |
dc.subject.mesh | Reverse Transcriptase Polymerase Chain Reaction | |
dc.subject.mesh | Signal Transduction | |
dc.subject.mesh | Apoptosis | |
dc.subject.mesh | Cell Proliferation | |
dc.subject.mesh | Glucose Transporter Type 1 | |
dc.subject.mesh | Hypoxia-Inducible Factor 1, alpha Subunit | |
dc.subject.mesh | Nanoparticles | |
dc.subject.mesh | Real-Time Polymerase Chain Reaction | |
dc.subject.mesh | Hypoxia | |
dc.title | Silver nanoparticles inhibit the function of hypoxia-inducible factor-1 and target genes: insight into the cytotoxicity and antiangiogenesis. | |
dc.type | Journal Article | |
utslib.citation.volume | 11 | |
utslib.location.activity | New Zealand | |
utslib.for | 0601 Biochemistry and Cell Biology | |
utslib.for | 1007 Nanotechnology | |
utslib.for | 1115 Pharmacology and Pharmaceutical Sciences | |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Mathematical and Physical Sciences | |
utslib.copyright.status | open_access | * |
dc.date.updated | 2022-08-15T21:49:27Z | |
pubs.publication-status | Published online | |
pubs.volume | 11 |
Abstract:
Hypoxia-inducible factor-1 (HIF-1) is a transcription factor that is activated upon exposure to hypoxic stress. It modulates a number of cellular responses including proliferation, apoptosis, angiogenesis, and metabolism by activating a panel of target genes in response to hypoxia. The HIF-1 level is often upregulated in the hypoxic microenvironment of solid tumors, which contributes to cancer treatment failure. Here we report that silver nanoparticles (AgNPs), which are widely used as an antimicrobial agent, are an effective inhibitor of HIF-1. AgNPs inhibited the activation of a HIF-dependent reporter construct after the cells were exposed to hypoxic conditions or treated with cobalt chloride, a hypoxia mimetic agent. The AgNPs also interfered with the accumulation of HIF-1α protein and the induction of the endogenous HIF target genes, VEGF-A and GLUT1. Since both HIF-1 and vascular endothelial growth factor-A play an important role in angiogenesis, AgNPs also inhibited angiogenesis in vitro. Our data reveal a new mechanism of how AgNPs act on cellular function, that is, they disrupt HIF signaling pathway. This finding provides a novel insight into how AgNPs can inhibit cancer cell growth and angiogenesis.
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