Abstract
Background/Aim
Upregulation of Forkhead box G1 (FOXG1) has recently been observed in many cancers, while its effect on radiosensitivity in glioma is still unclear. In this study, we hypothesized that FOXG1 be a major player in radioresistance of glioma as well as the underlying mechanism.
Methods
Immunohistochemistry (IHC) was conducted to assess FOXG1 expression in glioma tissues and glioma-adjacent tissues. Western Blot was implemented to detect the expression of autophagy-related proteins. CCK-8, colony formation and flow cytometry assays were implemented to assess cell viability, proliferation and apoptosis, respectively. Transmission electron microscope (TEM) was used to observe autophagic vesicles. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assay was applied to detect the expression of FOXG1.
Results
The present study demonstrated that FOXG1 was highly expressed in glioma tissues. FOXG1 expression level was up-regulated in glioma cells following exposure to X-ray irradiation. FOXG1 can attenuate radiosensitivity of glioma cells. Moreover, it revealed that FOXG1 attenuate radiosensitivity of glioma cells by promoting autophagy.
Conclusions
The present study suggests that FOXG1 is a pivotal molecule for circumventing radiation-induced cell death in malignant glioma cells through the regulation of autophagy, and it may be a target for the treatment of human brain glioma.
Acknowledgments
Not applicable.
Authors’ contributions
Ning Xiao and Min Hong reorganized the research and contributed to the revision and monitoring of the research during manuscript revision. Churong Li and Wenjun Liao proposed the hypothesis, analyzed the results, and wrote the manuscript. Wenjun Liao and Churong Li designed and executed the majority of the experiments. Jun Yin, Shichuan Zhang, and Peng Zhang, assisted in the execution of a part of the experiments. All authors read and approved the final version of the manuscript.
Ethics approval and consent to participate
The present study was approved by the Ethics Review Board of The University of Electronic Science and Technology of China, and written informed consent was obtained from all patients.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Availability of data and materials
The datasets used or analyzed during the present study are available from the corresponding author.