| Popis: |
Background: Radioresistance has a great impact on prognosis of glioma patients. However, the potential mechanism underlying the radioresistance of glioma cells remains largely unknown. Methods: LRIG1 overexpression model was firstly established by using Flag-LRIG1 plasmid. The expression of LRIG1, CTLA-4 proteins were detected by western blot and IHC in cells and human tissue. Real-time PCR was used for deterring mRNA expression. Cell viability and apoptosis were detected using CCK-8 and Annexin-V/propidium iodide (PI), respectively. Co-Immunoprecipitation was used for detecting the combination of LRIG1 and CTLA-4 proteins. Results: LRIG1 was significantly down-regulated in radioresistant glioma cells. Overexpressed LRIG1 could promote the radiosensitivity of glioma cells, meanwhile, inhibit the expression of p-AKT and CTLA-4 protein in radioresistant glioma cells. Furthermore, LRIG1 combined with CTLA-4 and promoted CTLA-4 degradation. In human glioma tissue, LRIG1 was down-regulated, while CTLA-4 was highly expressed in glioma tissue. Finally, correlation analysis showed that the expression of LRIG1 was negatively correlated with expression of CTLA-4 and radioresistance of glioma patients. Conclusion: Our findings demonstrated that LRIG1 facilitates radioresistance glioma cells by regulating CTLA4 /AKT signaling pathway. |
