Necessary for centrosome duplication at different stages of procentriole formation. Acts as a key negative regulator of ciliogenesis in collaboration with CEP97 by capping the mother centriole thereby preventing cilia formation (PubMed:23141541). Also involved in promoting ciliogenesis. May play a role in the assembly of the mother centriole subdistal appendages (SDA) thereby effecting the fusion of recycling endosomes to basal bodies during cilia formation (PubMed:26965371). Required for correct spindle formation and has a role in regulating cytokinesis and genome stability via cooperation with CALM1 and CETN2 (By similarity). Interacts with CALM1, CETN2, CEP76, CEP97, CEP104, CEP290, TALPID3. Seems to associate with discrete CETN2, CEP97 and CEP290-containing complexes. Interacts with NEURL4 and CCNF; these interactions are not mutually exclusive and both lead to CCP110 ubiquitination and proteasome-dependent degradation. Via its interaction with NEURL4, may indirectly interact with HERC2. Interacts with KIF24, leading to its recruitment to centrioles. Interacts with USP20 and USP33 (By similarity). Interacts with MPHOSPH9 (By similarity). Recruited early and then associates with the growing distal tips (PubMed:23141541). Recruited to the mother centriole by KIF24 (By similarity). Removed from centrioles by TTBK2, leading to initiation of ciliogenesis and localizes only to the daughter centriole in ciliated cells (PubMed:23141541). In cytotoxic T lymphocytes remains associated with the mother centriole during docking of the centrosome at the immunological synapse upon target contact (PubMed:26670998). Recruited at the distal end of the mother centriole by MPHOSPH9 (By similarity). Phosphorylated by CDKs. Ubiquitinated by the SCF(CCNF) during G2 phase, leading to its degradation by the proteasome and preventing centrosome reduplication. Deubiquitinated by USP33 in S and G2/M phase, leading to stabilize CCP110 during the period which centrioles duplicate and elongate (By similarity). Lethal within a few hours after birth with multiple defects in organogenesis. Mice show an early block in cilia formation and a phenotype reminiscent of human short rib-polydactyly syndrome.