Aurora kinase a suppresses metabolic stress-induced autophagic cell death by activating mTOR signaling in breast cancer cells

摘要: Aberrant Aur-A signaling is associated with tumor malignant behaviors. However, its involvement in metabolic stress not fully elucidated. In the present study, prolonged nutrient deprivation was conducted into breast cancer cells to mimic tumors. these cells, autophagy induced, leading caspase-independent cell death, which blocked by either targeted knockdown of autophagic gene ATG5 or inhibitor 3-Methyladenine (3-MA). overexpression mediated resistance death and promoted survival when exposed stress. Moreover, we provided evidence that suppressed a kinase-dependent manner. Furthermore, revealed enhanced mammalian target rapamycin (mTOR) activity under inhibiting glycogen synthase kinase 3β (GSK3β). Inhibition mTOR sensitized Aur-A-overexpressed stress-induced death. Consistently, presented an inverse correlation between expression (high) levels (low) clinical samples. conclusion, our data novel insight cyto-protective role against suppressing might help develop alternative avenues for therapy.