PRR11 (proline rich 11) is a critical cell cycle regulator that promotes oncogenic processes across multiple cancer types. The protein plays a fundamental role in cell cycle progression, particularly facilitating G1/S phase transition through regulation of cyclins like CCNE 1. PRR11 demonstrates periodic, cell cycle-dependent expression and its silencing causes significant S phase arrest and growth retardation 2. Mechanistically, PRR11 is regulated through a FBXW7/GSK3β-mediated ubiquitination pathway, where GSK3β phosphorylates PRR11's CDC4 phosphodegron motif, enabling FBXW7-catalyzed degradation 3. PRR11 creates positive feedback loops with AKT signaling to maintain its stability and promote tumor progression 3. The gene is consistently overexpressed in lung, breast, bladder, and renal cancers, where high expression correlates with poor prognosis 241. PRR11 promotes cellular proliferation, migration, invasion, and epithelial-mesenchymal transition while inhibiting apoptosis 1. Notably, PRR11 confers therapeutic resistance by stabilizing DHODH and preventing ferroptosis in glioblastoma 5. PRR11 forms a bidirectional transcription unit with SKA2, regulated by NF-Y and p53, representing a coordinated oncogenic module 64. These findings establish PRR11 as a promising therapeutic target with potential clinical applications in cancer treatment.