GLIPR1 regulates the TIMP1-CD63-ITGB1-AKT signaling pathway in glioma cells and induces malignant transformation of astroglioma

Background: Astrocytoma (ACM) is characterized by high recurrence rate, high mortality, and extremely poor clinical prognosis. The new diagnostic and prognostic tumor markers related to ACM was found to improve the diagnosis rate and reduce the poor prognosis. Methods: The activity of SHC-44 and SW1783 cells under the regulation of glioma pathogenesis-related protein 1 (GLIPR1) was investigated by CCK8 analysis. The effect of GLIPR1 on the proliferation of SHC-44 and SW1783 cells was analyzed by cell colony-forming experiment. The migration of SHC-44 and SW1783 cells under the regulation of GLIPR1 was analyzed by transwell assay. The effects of GLIPR1 on the invasion and migration of SHC-44 and SW1783 cells were analyzed by cell scratch test and transwell assay. Immunofluorescence and Co-IP assays were employed to analyze the expression characteristics of GLIPR1 and CD63 proteins. The effect of GLIPR1 on the protein expression of GLIPR1, TIMP1, CD63, ITGB1, and AKT in SHC-44 and SW1783 cells was analyzed by western blot. The effect of anti-AKT on the protein expression of GLIPR1, TIMP1, CD63, ITGB1, and AKT in SHC-44 and SW1783 cells was performed by western blot. Results: The outcomes revealed that GLIPR1 could enhance the activity, proliferation, migration, and invasion of ACM cells, which might be associated with the activation of the TIMP1-CD63-ITGB1-AKT signaling pathway. Conclusions: Taken together, GLIPR1 might be a potential target for the prevention or management of ACM in the clinic.