Centrosome clustering is essential for the survival of cells containing supernumerary centrosomes. Rhys et al. show that centrosome clustering is a two-step mechanism in which increased cortical contractility, driven by loss of E-cadherin, restricts centrosome movement, facilitating HSET-mediated clustering.

The presence of supernumerary centrosomes is a hallmark of human tumours. Recent work in animal models suggests that extra centrosomes are not just bystanders in cancer but can accelerate tumourigenesis in the absence of the tumour suppressor p53. Centrosome amplification could indeed actively participate in tumour progression through the induction of chromosome instability, disruption of tissue architecture and promoting cell invasion. Paradoxically, however, centrosome amplification is rather poorly tolerated in normal cells and there are several hurdles cells need to overcome in order to efficiently proliferate in the presence of extra centrosomes. Here, we review the adaptation mechanisms that allow cells to efficiently divide in the presence of extra centrosomes and how these could be exploited to develop selective cancer therapies.