Adhesion-growth factor crosstalk regulates AURKB activation and ERK signalling in re-adherent fibroblasts

Aurora kinases despite their similarity have distinct roles in the cell cycle, which is regulated by cell-matrix adhesion and growth factors. This study reveals loss of adhesion and re-adhesion to differentially regulate Aurora kinases. AURKB activation that drops on the loss of adhesion recovers on re-adhesion in serum-deprived conditions but not in the presence of serum growth factors. A rapid 30 min serum treatment of serum-deprived cells blocks the adhesion-dependent recovery of AURKB, which negatively correlates with Erk activation. AZD mediated inhibition of AURKB in serum-deprived re-adherent cells promotes Erk activation and membrane ruffling, comparable to presence of serum. These studies thus define a novel adhesion-growth factor-dependent regulation of AURKB that controls adhesion-dependent Erk activation in re-adherent fibroblasts.

Automated summary

Aurora kinases play distinct roles in the cell cycle, regulated by cell-matrix adhesion and growth factors. The activation of AURKB is different when cells lose adhesion and undergo re-adhesion, depending on the presence of serum growth factors. Adhesion-dependent Erk activation in re-adherent fibroblasts is controlled by a novel mechanism involving adhesion-growth factor-dependent regulation of AURKB.