CDCA3 is a cell cycle regulator that functions as an F-box-like protein required for mitosis entry 1. It participates in E3 ligase complexes that mediate ubiquitination and degradation of cell cycle regulators, with its activity modulated by casein kinase 2 and the APC/C-Cdh1 complex 2. CDCA3 is significantly overexpressed across multiple cancer types and serves as an independent prognostic biomarker 1. In bladder cancer, CDCA3 operates within a positive feedback loop with MYC transcription factor, wherein CDCA3 recruits TRIM28 to stabilize MYC, while MYC reciprocally upregulates CDCA3 3. This regulatory axis promotes cancer progression by enhancing glycolysis through ENO1 upregulation 3. CDCA3 is also transcriptionally activated by MYBL2 and FOXM1, which promote bladder cancer proliferation and metastasis, potentially through Wnt/β-catenin pathway activation 4. CDCA3 overexpression correlates with poor survival outcomes and advanced disease stage in prostate cancer and kidney renal papillary cell carcinoma 5, 6. Notably, elevated CDCA3 levels enhance sensitivity to platinum-based chemotherapy in non-small cell lung cancer through genome instability mechanisms, suggesting therapeutic potential when combined with CK2 inhibitors 2. CDCA3 is also implicated in premature ovarian failure and dry eye disease pathogenesis through cell cycle dysregulation 7.