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Proposed model of RNASE4-mediated promotion of GBM oncogenesis through AXL/AKT and NF-κB/cIAPs signaling activation under hypoxia. RNASE4 expression is induced under hypoxic conditions, leading to the activation of the AXL/AKT and NF-κB/cIAP1/cIAP2/SURVIVIN signaling pathways. These cascades, in turn, promote glioblastoma proliferation, epithelial-to-mesenchymal transition (EMT), stemness, and chemoresistance.
