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Cell viability at 0, 12, and 24 hr after exposure of miR-17-5p or miR-130b-3p mimics- or inhibitors-transfected SU3 cells to 10 Gy irradiation. The time of transfection with miR mimics, miR inhibitors, or NC miRs was 24 hr. Data were presented as mean ± SD of six independent experiments. ∗P<0.05, ∗∗P<0.01 vs. the control group at 0 (red), 12 (blue), and 24 hr (green) after irradiation; #P<0.05 vs. the 10 Gy + Mimic negative control group at 12 (blue) and 24 hr (green) after irradiation; &P<0.05 vs. the 10 Gy + Inhibitor negative control group at 12 (blue) and 24 hr (green) after irradiation. There was no obvious difference between the 10 Gy group and the 10 Gy + mimic negative control group or the 10 Gy + inhibitor negative control group.
Source publication
Background. The radioresistance of glioma stem cells (GSCs) is related to some microRNAs (miRs) generated by radiation. This study aimed to investigate the effects of miR-17-5p and miR-130b-3p on the radiosensitivity of GSCs. Methods. miR-17-5p and miR-130b-3p expressions in SU3 and SU3-5R cells were determined. SU3 cells transfected with miR-17-5p...
Citations
... About 30 mg of the tumor tissues was used to extract the proteins, and the levels of PTEN, HIF-1α, GLUT-1/3, VEGF, and β-actin protein expression in tumor tissues were determined by the western blot method according to previous description [15]. The dilution ratios of the primary antibodies were 1:1000 for HIF-1α, VEGF, GLUT-1, and GLUT-3; and 1:2000 for PTEN and β-actin. ...
... After transfection of SU3 cells with miR mimics or negative control miR, the cells in the miR-17-5p or miR-130b-3p mimics + vitexin + radiation groups were treated with the different concentrations of vitexin for 24 h, the cells in the radiation-treated groups then exposed to 10 Gy irradiation. The cell viability at 12 or 24 h after irradiation was measured by the MTT assay [15], and the expression levels of PTEN and HIF-1α proteins at 12 h after irradiation were measured by the western blot method. ...
... PTEN is a target gene of some miRs [3,4], it can change the radiosensitivity of glioma cells by negatively regulating the expression of HIF-1α [24,25]. Some previous studies have confirmed that miR-17-5p or miR-130b-3p can directly bind with the target gene PTEN [15,26,27]. To further investigate the inhibitory mechanisms of HIF-1α by vitexin, the expression levels of PTEN, miR-17-5p, and miR-130b-3p in tumor tissues were examined in this study. ...
Purpose
Vitexin can cooperate with hyperbaric oxygen to sensitize the radiotherapy of glioma by inhibiting the hypoxia-inducible factor (HIF)-1α. However, whether vitexin has a direct radiosensitization and how it affects the HIF-1α expression remain unclear. This study investigated these issues.
Methods
The SU3 cells-inoculated nude mice were divided into control, radiation, and vitexin + radiation groups. The vitexin + radiation-treated mice were intraperitoneally injected with 75 mg/kg vitexin daily for 21 days. On the 3rd, 10th, and 17th days during the vitexin treatment, the radiation-treated mice were locally irradiated with 10 Gy, respectively. In vitro, the microRNA (miR)-17-5p or miR-130b-3p mimics-transfected SU3 cells were used to examine the effects of vitexin plus radiation on expression of miR-17-5p- or miR-130b-3p-induced radioresistance-related pathway proteins. The effects of vitexin on miR-17-5p and miR-130b-3p expression in SU3 cells were also evaluated.
Results
Compared with the radiation group, the tumor volume, tumor weight, and expression of HIF-1α, vascular endothelial growth factor, and glucose transporter-1/3 proteins, miR-17-5p, and miR-130b-3p in tumor tissues in the vitexin + radiation group decreased, whereas the expression of phosphatase and tensin homolog (PTEN) protein increased. After treatment of miR-17-5p or miR-130b-3p mimics-transfected SU3 cells with vitexin plus radiation, the PTEN protein expression also increased, the HIF-1α protein expression decreased correspondingly. Moreover, vitexin decreased the miR-17-5p and miR-130b-3p expression in SU3 cells.
Conclusion
Vitexin can enhance the radiosensitivity of glioma, and its mechanism may partly be related to the attenuation of HIF-1α pathway after lowering the inhibitory effect of miR-17-5p and miR-130b-3p on PTEN.
