CCNB2 (cyclin B2) is a cell cycle regulator essential for G2/M transition control, functioning as a regulatory subunit of cyclin-dependent kinase complexes 1. Its expression is tightly regulated by multiple transcriptional mechanisms: circadian clock protein PER2 enhances CCNB2 transcription through HIF-1α-mediated pathway activation 2, while HMGA proteins directly bind the CCNB2 promoter to upregulate expression 1. CCNB2 also functions in preserving hematopoietic stem cell quiescence through chr15 remodeling mechanisms 3. CCNB2 overexpression is pathologically significant across multiple cancer types. In pituitary adenomas, CCNB2 upregulation facilitates cell cycle progression and inhibits apoptosis 21. In gastric cancer, CCNB2 promotes proliferation, migration, and epithelial-mesenchymal transition via PI3K/AKT pathway activation 4. CCNB2 elevation associates with poor prognosis in hepatocellular carcinoma, correlating with disease recurrence and WHO grade 56. In low-grade glioma, CCNB2 expression predicts poorer overall survival and correlates with immune cell infiltration 7. Additionally, CCNB2 involvement in psoriasis suggests dysregulation of cell cycle control contributes to aberrant immune-mediated inflammation 8.