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. Author manuscript; available in PMC: 2020 May 6.
Published in final edited form as: Dev Cell. 2019 May 6;49(3):325–331. doi: 10.1016/j.devcel.2019.04.002

Figure 1. Mechanisms by which centrosome aberrations can promote invasive phenotypes.

Figure 1.

A. Centrosome amplification induced by Plk4 overexpression leads to increased microtubule nucleation and dynamics. This increases Rac1 signaling (1), resulting in the activation of the Arp2/3 complex (2), increased actin polymerization (3), and weakening of E-cadherin junctions (4) to promote the formation of invasive protrusions (invadopodia) in cells with extra centrosomes.

B. Pro-invasive factors secreted from cells with extra centrosomes promote the formation of invadopodia in cells with normal centrosome numbers. This extra centrosomes-associated secretory pathway (ECASP) is dependent on elevated reactive oxygen species in cells with amplified centrosomes. The secreted pro-invasive factors activate receptors (1), leading to increased Rac1 signaling (2), activation of the Arp2/3 complex (3), increased actin polymerization (4), and weakening of E-cadherin junctions (5) to promote invadopodia formation in cells with normal centrosome numbers.

C. Structural centrosome aberrations induced by overexpression of Nlp lead to increased microtubule nucleation and stability. This increases interphase cell stiffness and disrupts E-cadherin junctions, promoting the selective extrusion of softer mitotic cells from the epithelium.

D. Structural centrosome aberrations induced by overexpression of Nlp and CEP131 promote basal extrusion of damaged cells.