Laboratory experiments reveal quercetin activates the UBC6 enzyme, which orchestrates a cascade that degrades AURKA protein and activates AMPK signaling in ovarian cancer cells. This mechanism reduced tumor growth by 60% and blocked metastasis in mouse models through enhanced protein ubiquitination pathways. The finding connects quercetin's anti-cancer effects to a specific molecular target previously uncharacterized in ovarian malignancy. This mechanistic clarity could explain why population studies show reduced ovarian cancer risk among women consuming quercetin-rich foods like onions, apples, and green tea. The UBC6-PRKN-AURKA axis represents a promising therapeutic vulnerability, as AURKA overexpression drives aggressive ovarian cancer phenotypes in roughly 80% of cases. However, translation faces significant hurdles. Quercetin's poor bioavailability requires high doses that may cause gastrointestinal distress, and the current research used cell lines that may not reflect tumor heterogeneity. The mouse model, while promising, used immunocompromised animals that cannot assess immune system interactions. Still, identifying UBC6 as quercetin's primary target opens avenues for developing more potent synthetic analogs or combination therapies targeting this ubiquitination pathway.