CCNY (cyclin Y) functions as a positive regulatory subunit of cyclin-dependent kinases CDK14/PFTK1 and CDK16, serving as a key cell-cycle regulator 1. During G2/M phase transition, CCNY recruits CDK14/PFTK1 to the plasma membrane and promotes phosphorylation of LRP6, thereby activating Wnt signaling pathway 1. CCNY also acts as an actin-binding protein that modulates actin dynamics and inhibits cofilin activation 1. In cancer biology, CCNY expression significantly promotes cell migration and invasion activity in vitro and in vivo 1. In non-small cell lung cancer (NSCLC), CCNY-mediated phosphorylation of PRC1 (protein regulator of cytokinesis 1) is essential for tumor progression, with silencing CCNY reducing cell growth, impairing spindle formation, and promoting G2/M phase arrest 2. Tissue microarray analyses reveal elevated CCNY levels correlate with unfavorable prognosis in NSCLC patients, suggesting CCNY as a promising therapeutic target 2. Additionally, CCNY may participate in MYC-mediated transcription activation through its isoform 3, and positively regulates autophagy, though these functions require further characterization.