CETN3 is a calcium-binding centrin protein with dual roles in centrosome assembly and RNA processing. As a component of the TREX-2 complex, CETN3 mediates mRNA export from the nucleus through nuclear pores 1. At the centrosome, CETN3 functions as a negative regulator of the Mps1 kinase, inhibiting its autophosphorylation and antagonizing centrin 2-dependent centriole assembly and centrosome duplication 2. Additionally, CETN3 participates in RNA splicing regulation; the CETN3-S splice isoform is controlled by SRSF2 and promotes colorectal cancer cell proliferation through G1/S cell cycle progression 3. Loss of CETN3 function causes primary microcephaly through impaired centrosome assembly in neural stem/progenitor cells and disrupted interaction with RNA splicing machinery critical for brain development 4. In cancer, CETN3 loss via 5q deletion in basal-like breast cancer correlates with elevated EGFR signaling 15, while miR-410 negatively regulates CETN3 expression to promote tumorigenesis in certain contexts 6. These findings establish CETN3 as a multifunctional regulator linking centrosome dynamics, RNA metabolism, and neurodevelopment, with emerging roles in cancer biology.