The control of cell cycle progression was shown to be associated with maintenance of genomic fidelity.Defects in regulation of cell cycle progression may result in genomic instabilities, including gene mutation, amplification, or chromosomal aberrations, which were associated with malignant transformation and tumorigenesis.In addition, inactivation of cell cycle control could also have dramatic consequences on therapeutic sensitivity.We showed that tumor suppressor BRCA1 physically interacted and colocalized with Nlp (Nineinlike protein).Interestingly, Nlp centrosomal localization likely depended on normal cellular BRCA1 function because cells containing BRCA1 mutations or silenced for endogenous BRCA1 revealed disrupted Nlp colocalization to centrosomes.