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. Author manuscript; available in PMC: 2016 Jan 31.
Published in final edited form as: Trends Cell Biol. 2014 Nov 7;25(2):65–73. doi: 10.1016/j.tcb.2014.10.002

Figure 5. Cancer-associated molecular drivers of abnormal centrosome dynamics.

Figure 5

Usp44 knockout and cyclin B2 overexpression cause spontaneous tumors in mice and feature delayed and accelerated centrosome separation, respectively [4, 5]. p53 inactivation also causes abnormal centrosome disjunction and is the most commonly mutated tumor suppressor in human cancers. It is likely that there are many other proteins, such as the CIN70 gene Nek2A [96], that regulate centrosome disjunction that, when altered, promote CIN and may be associated with cancer. Likewise, abnormal centrosome movement, as is the case for Eg5 overexpression, is tightly associated with CIN and tumorigenesis. There remains a critical need to identify other cancer-associated genes that normally regulate centrosome dynamics.