Background: It is well documented that low dose ionizing radiation induces migration of glioma cells, but the mechanisms are still poorly understood. The aim of the current study was to elucidate the intracellular signal transduction pathways of radiation induced migration in human glioma cells. Methods:Migration was assessed via a wound healing assay. In addition, tumor cell proliferation was evaluated with a MTT colorimeritric assay using 3 glioma cell lines (LN18, LN229, LNZ308). The cells were treated with increasing doses of irradiation (2Gy, 5Gy, 8Gy) in the presence or absence of EGF or inhibitors of the EGFR or downstream pathways (AG1478, LY294002, PD98059). Biochemical activation of EGFR, Akt/PKB and MAPK/ERK was examined by Western blot analysis.Results: Irradiation induced a dose dependant intense increase of migrating cells and a decrease of proliferation. The inhibition of PI3K by LY294002 (50 µmol/L) reduced the radiation-induced migration (LN18: p<0.001, LN229: p=0.16, LNZ308: p=0.13), the blockade of MEK1 by PD98059 (50 µmol/L) was also effective (LN18: p=0.036, LN229: p=0.021, LNZ308: p=0.021). After irradiation, no effect on EGFR or the downstream pathways was observed in Western blot analysis. Conclusion:Our results demonstrate that the downstream pathways of EGFR are involved in radiation induced migration of glioma cells.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.