Glioblastoma (GBM) is a highly invasive and malignant primary intracranial tumor originating from glial cells, and it is associated with an extremely poor clinical prognosis. The hypoxic conditions within GBM promote various tumor cell processes such as angiogenesis, proliferation, migration, invasion, and drug resistance. A key aspect of tumor adaptation to the hypoxic environment and the promotion of malignant behaviors is the regulation of HIF-1α signaling pathways. However, the specific pathogenic mechanisms involving HIF-1α in GBM have not been thoroughly investigated. This study reveals significant overexpression of both HIF-1α and CD47 in GBM. Patients with high HIF-1α levels and CD47 expression had significantly reduced overall survival and disease-free survival times. Furthermore, a positive correlation was observed between the expression levels of HIF-1α and CD47 in GBM. Lentivirus-mediated knockdown of HIF-1α protein and plasmid-based overexpression of CD47 protein simultaneously enhanced cell proliferation, clonogenic potential and cell migration abilities in GBM, and HIF-1α was found to regulate key pathways, including the P-PI3K/P-AKT, SOX2/OCT4 and MMP2/MMP9 pathways, in GBM.
Keywords: CD47; HIF-1α; glioblastoma; migration; proliferation.
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