“…However, how Aurora-A is activated is not fully understood. Some activators of Aurora-A are known, including the LIM-domain protein Ajuba ( Goyal et al, 1999 ; Hirota et al, 2003 ), the microtubule-associated protein TPX2 ( Eyers et al, 2003 ), p21-activated protein kinase 1 (Pak1) ( Zhao et al, 2005 ), thyroid hormone receptor-associated protein complex component/methyl-CpG binding endonuclease TRAP220/MED1 ( Udayakumar et al, 2006 ), EGFR ( Hung et al, 2008 ; Lai et al, 2010 ), ubiquitin-specific processing protease-7 (USP7) ( Giovinazzi et al, 2013 ), a classic tumor suppressor p53 ( Yang et al, 2018 ), heterogeneous nuclear ribonucleoprotein Q1 protein (HnRNP Q1) ( Lai et al, 2018 ), the receptor of activated C-kinase1 (RACK1) ( Shen et al, 2019 ), the NE proteins containing the LEM domain LEM4 ( Gao et al, 2018 ), and KIAA1529 ( Qiao et al, 2022 ). Most notably, EGF can increase Aurora-A gene expression through the nuclear EGFR/STAT5 signaling pathway and ultimately lead to chromosome instability and tumorigenesis ( Hung et al, 2008 ).…”