Back to Search Start Over

Pulsed and Discontinuous Electromagnetic Field Exposure Decreases Temozolomide Resistance in Glioblastoma by Modulating the Expression of O6-Methylguanine-DNA Methyltransferase, Cyclin-D1, and p53.

Authors :
Dehghani-Soltani, Samereh
Eftekhar-Vaghefi, Seyed Hassan
Babaee, Abdolreza
Basiri, Mohsen
Mohammadipoor-ghasemabad, Lily
Vosough, Parisa
Ahmadi-Zeidabadi, Meysam
Source :
Cancer Biotherapy & Radiopharmaceuticals. Sep2021, Vol. 36 Issue 7, p579-587. 9p.
Publication Year :
2021

Abstract

Background: Glioblastoma is a malignant and very aggressive brain tumor with a poor prognosis. Despite having chemotherapy concomitant with surgery and/or radiation therapy, the median survival of glioblastoma-affected people is less than 1 year. Temozolomide (TMZ) is a chemotherapeutic used as a first line treatment of glioblastoma. Several studies have reported that resistance to TMZ due to overexpression of O6-methylguanine-DNA methyltransferase (MGMT) is the main reason for treatment failure. Several studies described that pulsed-electromagnetic field (EMF) exposure could induce cell death and influence gene expression. Materials and Methods: In this study the authors assessed the effects of EMF (50 Hz, 70 G) on cytotoxicity, cell migration, gene expression, and protein levels in TMZ-treated T98 and A172 cell lines. Results: In this study, the authors show that treatment with a combination of TMZ and EMF enhanced cell death and decreased the migration potential of T98 and A172 cells. The authors also observed overexpression of the p53 gene and downregulation of cyclin-D1 protein in comparison to controls. In addition, T98 cells expressed the MGMT protein following treatment, while the A172 cells did not express MGMT. Conclusion: Their data indicate that EMF exposure improved the cytotoxicity of TMZ on T98 and A172 cells and could partially affect resistance to TMZ in T98 cells. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
10849785
Volume :
36
Issue :
7
Database :
Academic Search Index
Journal :
Cancer Biotherapy & Radiopharmaceuticals
Publication Type :
Academic Journal
Accession number :
152352328
Full Text :
https://doi.org/10.1089/cbr.2020.3851