Table 1 Top hits for drivers of centrosome amplification in human cancer.

From: Analysis of the “centrosome-ome” identifies MCPH1 deletion as a cause of centrosome amplification in human cancer

Centrosome gene

Known functions (especially centrosome-related functions)

Hypothesis

CEP19

Ciliation; microtubule anchoring to the centrosome; inactivation results in morbid obesity

Gain of function causes CA

CEP72

Centriolar satellite component; recruit key centrosomal proteins to centrosome; microtubule nucleation; BRCA1 interactor; overexpression increases CIN, aneuploidy, lagging chromosomes

Gain of function causes CA

CEP76

Limits centriole duplication; depletion drives aberrant amplification of centrioles

Loss of function causes CA

CTNNB1

Wnt signaling pathway; negative regulator of centrosome cohesion; overexpression of stabilized mutant increases centrosomes

Gain of function causes CA

MCPH1

Neurogenesis; chromosome condensation; DNA damage response; restrains DNA damage-induced CA; germline mutations cause microcephaly

Loss of function causes CA

NEURL4

Interacts with CP110 (important for limiting centriole elongation)

Loss of function causes CA

NDRG1

Cell trafficking; regulates centrosome number

Gain of function causes CA

NPM1

Ribosome biogenesis; depleting NPM1 results in CA

Loss of function causes CA

PTK2

Cell migration, adhesion, spreading, actin reorganization, focal adhesion formation, proliferation, apoptosis

Gain of function causes CA

SPATC1

Proximal centriole marker

Gain of function causes CA

TBCCD1

Localizes to a region sub-proximal to centrioles; mutant cells have variable numbers of centrioles and centriole positioning defects required for mother-daughter centriole linkage and mitotic spindle orientation; migration

Gain of function causes CA