Therefore, as a potential tumor suppressor, AP-2α inhibits the tumor sphere formation, self-renewal and intracranial tumor formation capacities of GSCs by regulating the Nanog/Sox2/CD133 signaling axis, suggesting that AP-2α is responsible for the maintenance of stem cell-like tumor growth, and could serve as a prime therapeutic target for the treatment of glioma. Here, PROM1 is linked to central nervous system cancer.