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For instance, ROS exposure in HLE and SNU cells upregulates cyclin D1 and activates the PI3K/AKT pathway, effects that are completely abolished by N-acetylcysteine or catalase, confirming their ROS dependency[89]

The tumor classification based on SSP activation patterns reveals that the conserved mechanisms of SSP, including redox homeostasis maintenance, one-carbon metabolism and drug resistance regulation, can serve as universal targets for pan-cancer therapeutic interventions

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