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Notably, breast cancer cells achieve metabolic adaptation by hijacking the autophagy mechanism: under glucose-deprivation conditions, MANF-mediated mitophagy eliminates dysfunctional mitochondria through the PRKN/Parkin-dependent pathway, maintains the ATP supply and promotes tumour survival [112], suggesting that targeting the MANFPRKN interaction can break the drug resistance barrier of breast cancer under metabolic stress
Beyond acting as carriers, certain metal-based NPs exhibit intrinsic anti-inflammatory activity and can function as therapeutic agents without encapsulating additional drugs or requiring external stimuli such as heat, magnetic fields, or light [40]
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They are not easily broken by heating or high salt concentration and require high activation energies
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