PCIF1 modulates glioblastoma cell migration and invasion by altering PI(3,4)P2 levels through the PI5-phosphatase INPP5B

• PCIF1 suppresses glioblastoma cell migration and invasion by inhibiting EMT, as evidenced by changes in mesenchymal and epithelial markers. • PCIF1 regulates AKT signaling through a dual mechanism: promoting proteasomal degradation of AKT while increasing p-AKT levels. • PCIF1 knockdown upregulates INPP5B, leading to PI(3,4)P2 accumulation and enhanced AKT activation, whereas overexpression increases PI(3,4,5)P3 and p-AKT. • PCIF1 is identified as a potential biomarker and therapeutic target for glioblastoma, offering new avenues for treatment.