CCNP (cyclin P) is an atypical cyclin involved in cell cycle regulation and cancer stemness. Functionally, CCNP localizes to the nucleus and cytoplasm where it acts as a cyclin-dependent protein kinase regulator, participating in G1/S transition of the mitotic cell cycle 1. CCNP appears to regulate cell proliferation and migration through its interaction with cyclin-dependent protein kinase holoenzyme complexes. Mechanistically, CCNP promotes cancer stemness by activating the WNT signaling pathway 1. Overexpression of CCNP increases spheroid formation in breast, lung, and colorectal cancer cell lines and upregulates stemness markers (CD44, CD133) and pluripotency factors (SOX2, OCT4, NANOG) 1. Additionally, CCNP induces multidrug resistance by promoting expression of ATP-binding cassette transporters, and CCNP knockout decreases OCT4 expression in induced-pluripotent stem cells 1. Clinically, CCNP upregulation correlates with poor prognosis in lung and colorectal cancers and is associated with chemoresistance 1. These findings identify CCNP as a novel therapeutic target in cancer, particularly for tumors exhibiting stem cell characteristics and drug resistance phenotypes.