ArticleCurrent health sciences journal
β-arrestin 1 Overexpression Increases Temozolomide Resistance in Human Malignant Glioma Cells.
Article in Current health sciences journal. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Research trends in glioma chemoradiotherapy resistance: a bibliometric analysis (2003-2023).Frontiers in oncology · 2025Article
- Glioblastoma pharmacotherapy: A multifaceted perspective of conventional and emerging treatments (Review).Experimental and therapeutic medicine · 2021Review
- The Effect of Β-Arrestin2 Overexpression Regarding Viability and Temozolomide Treatment in High-Grade Glioma Cells.Current health sciences journalArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many studies highlighted β-arrestins (β-arr) as essential proteins behind the regulation of major cell signaling pathways in different types of cancer. An impaired β-arrestin 1 (β-arr 1) activation/phosphorylation was suggested to be associated with a high malignant phenotype of glioma. Elevated levels of β-arrestin 2 (β-arr 2) mRNA were also found in advanced stages of breast cancer compared to early stages. In addition, β2-arrestin was also linked to a suppressive effect on tumor growth in other types of cancers such as prostate or non-small cell lung cancer. In this study, we analyzed the effect of β-arr 1 overexpression on the cytotoxic effect of Temozolomide (TMZ) in two malignant glioma (MG) cell lines: U-343MGa and Cl2:6. For this purpose, the cells were transected with β-arr 1 and then treated with different concentrations of TMZ for 24, 48 and 72 hours. At the end of the treatment, the cell viability was analyzed by Prestoblue viability assay. Our results showed that TMZ treatment induced cytotoxicity in MG cells while β-arr 1 transfection significantly reduced the TMZ cytotoxic effect in both U-343MGa and Cl2:6 MG cell lines. These results suggest that β-arr 1 overexpression may be a cause of TMZ resistance in MG.
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Registered trials
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