ArticleCancer gene therapy2014
In vitro and in vivo radiosensitization of human glioma U251 cells induced by upregulated expression of SLC22A18.
Article in Cancer gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Glioblastoma multiforme: an updated overview of temozolomide resistance mechanisms and strategies to overcome resistance.Discover oncology · 2025Review
- Current landscape and future directions of targeted-alpha-therapy for glioblastoma treatment.Theranostics · 2025Review
- Targeting Solute Carrier Transporters (SLCs) as a Therapeutic Target in Different Cancers.Diseases (Basel, Switzerland) · 2024Review
- Preclinical Models and Technologies in Glioblastoma Research: Evolution, Current State, and Future Avenues.International journal of molecular sciences · 2023Review
- Silencing SATB1 overcomes temozolomide resistance by downregulating MGMT expression and upregulating SLC22A18 expression in human glioblastoma cells.Cancer gene therapy · 2018Article
- Hyperoxygenation as a Therapeutic Supplement for Treatment of Triple Negative Breast Cancer.Frontiers in oncology · 2018Article
- SLC transporters as a novel class of tumour suppressors: identity, function and molecular mechanisms.The Biochemical journal · 2016Review
- Article
- Mouse models of glioblastoma for the evaluation of novel therapeutic strategies.Neuro-oncology advancesReview
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous study showed that solute carrier family 22 (organic cation transporter) member 18 (SLC22A18) downregulation via promoter methylation was associated with the development and progression of glioma, and the elevated expression of SLC22A18 was found to increase the sensitivity of glioma U251 cells to the anticancer drug 1,3-bis(2-chloroethyl)-1-nitrosourea. In this study, we investigated the possible upregulated expression of SLC22A18-induced enhancement of radiosensitivity of human glioma U251 cells in order to provide evidence in support of further clinical investigations. Stably overexpressing SLC22A18 human glioma U251 cells were generated to investigate the effect of SLC22A18 on the sensitivity of cells to irradiation in vitro using clonogenic survival assay. The apoptosis of U251 cells was examined with terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay. DNA damage and repair were measured using γH2AX foci. The effect of SLC22A18 on the in vivo tumor radiosensitivity was investigated in the orthotopic mice model. Upregulated expression of SLC22A18 enhanced the radiosensitivity of glioma U251 cells and also enhanced irradiation-induced apoptosis of U251 cells, but irradiation-induced apoptosis did not correlate with radiosensitizing effect of upregulated expression of SLC22A18. The repair of irradiation-induced double-strand-breaks was retarded in stably overexpressing SLC22A18 U251 cells. In the orthotopic mice model, the upregulated expression of SLC22A18 in U251 cells enhanced the effect of irradiation treatment and increased the survival time of mice. These results show that upregulated expression of SLC22A18 radiosensitizes human glioma U251 cells by suppressing DNA repair capacity.
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