The Effect of VPA on Increasing Radiosensitivity in Osteosarcoma Cells and Primary-Culture Cells from Chemical Carcinogen-Induced Breast Cancer in Rats.
- Publisher:
- MDPI
- Publication Type:
- Journal Article
- Citation:
- Int J Mol Sci, 2017, 18, (5), pp. E1027
- Issue Date:
- 2017-05-10
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Full metadata record
| Field | Value | Language |
|---|---|---|
| dc.contributor.author | Liu, G | |
| dc.contributor.author | Wang, H | |
| dc.contributor.author | Zhang, F | |
| dc.contributor.author | Tian, Y | |
| dc.contributor.author | Tian, Z | |
| dc.contributor.author | Cai, Z | |
| dc.contributor.author | Lim, D | |
| dc.contributor.author | Feng, Z | |
| dc.date.accessioned | 2024-09-03T23:31:18Z | |
| dc.date.available | 2017-05-05 | |
| dc.date.available | 2024-09-03T23:31:18Z | |
| dc.date.issued | 2017-05-10 | |
| dc.identifier.citation | Int J Mol Sci, 2017, 18, (5), pp. E1027 | |
| dc.identifier.issn | 1422-0067 | |
| dc.identifier.issn | 1422-0067 | |
| dc.identifier.uri | http://hdl.handle.net/10453/180603 | |
| dc.description.abstract | This study explored whether valproic acid (VPA, a histone deacetylase inhibitor) could radiosensitize osteosarcoma and primary-culture tumor cells, and determined the mechanism of VPA-induced radiosensitization. The working system included osteosarcoma cells (U2OS) and primary-culture cells from chemical carcinogen (DMBA)-induced breast cancer in rats; and clonogenic survival, immunofluorescence, fluorescent in situ hybridization (FISH) for chromosome aberrations, and comet assays were used in this study. It was found that VPA at the safe or critical safe concentration of 0.5 or 1.0 mM VPA could result in the accumulation of more ionizing radiation (IR)-induced DNA double strand breaks, and increase the cell radiosensitivity. VPA-induced radiosensitivity was associated with the inhibition of DNA repair activity in the working systems. In addition, the chromosome aberrations including chromosome breaks, chromatid breaks, and radial structures significantly increased after the combination treatment of VPA and IR. Importantly, the results obtained by primary-culture cells from the tissue of chemical carcinogen-induced breast cancer in rats further confirmed our findings. The data in this study demonstrated that VPA at a safe dose was a radiosensitizer for osteosarcoma and primary-culture tumor cells through suppressing DNA-double strand breaks repair function. | |
| dc.format | Electronic | |
| dc.language | eng | |
| dc.publisher | MDPI | |
| dc.relation.ispartof | Int J Mol Sci | |
| dc.relation.isbasedon | 10.3390/ijms18051027 | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.subject | 0399 Other Chemical Sciences, 0604 Genetics, 0699 Other Biological Sciences | |
| dc.subject.classification | Chemical Physics | |
| dc.subject.classification | 3101 Biochemistry and cell biology | |
| dc.subject.classification | 3107 Microbiology | |
| dc.subject.classification | 3404 Medicinal and biomolecular chemistry | |
| dc.subject.mesh | Animals | |
| dc.subject.mesh | Cell Line, Tumor | |
| dc.subject.mesh | Cells, Cultured | |
| dc.subject.mesh | Chromosome Aberrations | |
| dc.subject.mesh | DNA Breaks, Double-Stranded | |
| dc.subject.mesh | DNA Repair | |
| dc.subject.mesh | Female | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Mammary Neoplasms, Experimental | |
| dc.subject.mesh | Osteosarcoma | |
| dc.subject.mesh | Radiation Tolerance | |
| dc.subject.mesh | Radiation-Sensitizing Agents | |
| dc.subject.mesh | Rats | |
| dc.subject.mesh | Rats, Sprague-Dawley | |
| dc.subject.mesh | Valproic Acid | |
| dc.subject.mesh | Cells, Cultured | |
| dc.subject.mesh | Cell Line, Tumor | |
| dc.subject.mesh | Animals | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Rats | |
| dc.subject.mesh | Rats, Sprague-Dawley | |
| dc.subject.mesh | Osteosarcoma | |
| dc.subject.mesh | Mammary Neoplasms, Experimental | |
| dc.subject.mesh | Chromosome Aberrations | |
| dc.subject.mesh | Valproic Acid | |
| dc.subject.mesh | Radiation-Sensitizing Agents | |
| dc.subject.mesh | DNA Repair | |
| dc.subject.mesh | Radiation Tolerance | |
| dc.subject.mesh | Female | |
| dc.subject.mesh | DNA Breaks, Double-Stranded | |
| dc.subject.mesh | Animals | |
| dc.subject.mesh | Cell Line, Tumor | |
| dc.subject.mesh | Cells, Cultured | |
| dc.subject.mesh | Chromosome Aberrations | |
| dc.subject.mesh | DNA Breaks, Double-Stranded | |
| dc.subject.mesh | DNA Repair | |
| dc.subject.mesh | Female | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Mammary Neoplasms, Experimental | |
| dc.subject.mesh | Osteosarcoma | |
| dc.subject.mesh | Radiation Tolerance | |
| dc.subject.mesh | Radiation-Sensitizing Agents | |
| dc.subject.mesh | Rats | |
| dc.subject.mesh | Rats, Sprague-Dawley | |
| dc.subject.mesh | Valproic Acid | |
| dc.title | The Effect of VPA on Increasing Radiosensitivity in Osteosarcoma Cells and Primary-Culture Cells from Chemical Carcinogen-Induced Breast Cancer in Rats. | |
| dc.type | Journal Article | |
| utslib.citation.volume | 18 | |
| utslib.location.activity | Switzerland | |
| utslib.for | 0399 Other Chemical Sciences | |
| utslib.for | 0604 Genetics | |
| utslib.for | 0699 Other Biological Sciences | |
| pubs.organisational-group | University of Technology Sydney | |
| pubs.organisational-group | University of Technology Sydney/Faculty of Health | |
| pubs.organisational-group | University of Technology Sydney/Faculty of Health/IMPACCT | |
| pubs.organisational-group | University of Technology Sydney/All Manual Groups | |
| pubs.organisational-group | University of Technology Sydney/All Manual Groups/Improving Palliative, Aged and Chronic Care through Clinical Research and Translation (IMPACCT) | |
| pubs.organisational-group | University of Technology Sydney/All Manual Groups/UTS Ageing Research Collaborative (UARC) | |
| pubs.organisational-group | University of Technology Sydney/All Manual Groups/Digital, Virtual and AI in Health Collaborative (DVAIHC) | |
| utslib.copyright.status | open_access | * |
| dc.rights.license | This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/ | |
| dc.date.updated | 2024-09-03T23:31:13Z | |
| pubs.issue | 5 | |
| pubs.publication-status | Published online | |
| pubs.volume | 18 | |
| utslib.citation.issue | 5 |
Abstract:
This study explored whether valproic acid (VPA, a histone deacetylase inhibitor) could radiosensitize osteosarcoma and primary-culture tumor cells, and determined the mechanism of VPA-induced radiosensitization. The working system included osteosarcoma cells (U2OS) and primary-culture cells from chemical carcinogen (DMBA)-induced breast cancer in rats; and clonogenic survival, immunofluorescence, fluorescent in situ hybridization (FISH) for chromosome aberrations, and comet assays were used in this study. It was found that VPA at the safe or critical safe concentration of 0.5 or 1.0 mM VPA could result in the accumulation of more ionizing radiation (IR)-induced DNA double strand breaks, and increase the cell radiosensitivity. VPA-induced radiosensitivity was associated with the inhibition of DNA repair activity in the working systems. In addition, the chromosome aberrations including chromosome breaks, chromatid breaks, and radial structures significantly increased after the combination treatment of VPA and IR. Importantly, the results obtained by primary-culture cells from the tissue of chemical carcinogen-induced breast cancer in rats further confirmed our findings. The data in this study demonstrated that VPA at a safe dose was a radiosensitizer for osteosarcoma and primary-culture tumor cells through suppressing DNA-double strand breaks repair function.
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