C10orf90 is a tumor suppressor with dual roles in cell cycle checkpoint control and centrosomal function. As a p53 pathway regulator, C10orf90 exhibits E3 ubiquitin ligase activity and promotes p53 activation by inhibiting MDM2 binding and stimulating polyubiquitination through K11, K29, and K63 linkages 1. This enhances p53-dependent transcription of CDKN1A/p21, strengthening G2/M checkpoint responses to DNA damage 1. A functional variant (rs11245007) modulates C10orf90's E3 activity, with the 262N variant showing enhanced p53 polyubiquitination and stronger tumor suppression in multiparous women 1. At the centrosome, C10orf90 localizes to centrioles and participates in primary cilium assembly and centriole formation/stability 2. Disease relevance spans multiple cancers: C10orf90 expression varies across tumor types and correlates with prognosis, immune infiltration, and drug sensitivity 3. In colon cancer specifically, C10orf90 suppresses proliferation and migration while promoting apoptosis 3. Deletions in the 10q region encompassing C10orf90 correlate with metastasis risk in conjunctival melanoma 4. Downregulation occurs in benign ocular proliferative lesions (pterygium, pinguecula), suggesting involvement in early neoplastic pathways 5. C10orf90 represents a potential diagnostic and prognostic biomarker for cancer management.