Tetrandrine Exerts a Radiosensitization Effect on Human Glioma through Inhibiting Proliferation by Attenuating ERK Phosphorylation
| Autor: | Ji-Wei Ma, Jianxian Huang, Xueyun Zhong, Yu-Lin Wen, Ru Li, Yong Zhang, Ji-cheng Ye |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
MAPK/ERK pathway DNA repair Proliferation Tetrandrine Immunofluorescence Biochemistry 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Western blot Glioma Drug Discovery medicine Radiosensitization Pharmacology medicine.diagnostic_test biochemical phenomena metabolism and nutrition Cell cycle medicine.disease ERK 030104 developmental biology chemistry 030220 oncology & carcinogenesis Cancer research Molecular Medicine Phosphorylation Original Article |
| Zdroj: | Biomolecules & Therapeutics |
| ISSN: | 1976-9148 2005-4483 |
| DOI: | 10.4062/biomolther.2016.044 |
| Popis: | Tetrandrine (Tet), a bisbenzylisoquinoline alkaloid, has been reported to have a radiosensitization effect on tumors. However, its effects on human glioma and the specific molecular mechanisms of these effects remain unknown. In this study, we demonstrated that Tet has a radiosensitization effect on human glioma cells. It has been hypothesized that Tet has a radiosensitization effect on glioma cells by affecting the glioma cell cycle and DNA repair mechanism and that ERK mediates these activities. Therefore, we conducted detailed analyses of the effects of Tet on the cell cycle by performing flow cytometric analysis and on DNA repair by detecting the expression of phosphorylated H2AX by immunofluorescence. We used western blot analysis to investigate the role of ERK in the effect of Tet on the cell cycle and DNA repair. The results revealed that Tet exerts its radiosensitization effect on glioma cells by inhibiting proliferation and decreasing the expression of phosphorylated ERK and its downstream proteins. In summary, our data indicate that ERK is involved in Tet-induced radiosensitization of glioma cells via inhibition of glioma cell proliferation or of the cell cycle at G0/G1 phase. |
| Databáze: | OpenAIRE |
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