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1 Introduction Metabolic reprogramming stands as one of the hallmarks of malignant tumors, enabling tumor cells to remodel core metabolic pathways to meet the demands of rapid proliferation, invasion, metastasis, and adaptation to microenvironmental stress ( de novo synthesis pathway (SSP), which becomes the primary intracellular source of serine in tumor cells ( In recent years, with the advancement of pan-cancer studies, aberrant activation of the SSP has been successively identified across various malignant tumors, and its biological functions and regulatory mechanisms exhibit remarkable cancer-type heterogeneity ( Against this background, this review begins with the metabolic mechanism of the SSP, and elaborates in detail on its core functions in pan-cancer, multi-level regulatory networks, as well as current therapeutic strategies and challenges targeting the SSP, aiming to provide a reference for subsequent tumor metabolism research and clinical translation

This hydrogen peroxide reacts with ferrous ions to form hydroxyl radicals, which then transform the bis-allyl hydrogens in PUFAs into PUFA radicals

(2) Excessive inflammatory mediators trigger the infiltration of inflammatory cells, which then release a multitude of cytokines, such as transforming growth factors and fibroblast growth factors

Glutathion trgt zur Regeneration des antioxidativen Potenzials von Superoxiddismutase (SOD), Alpha-Liponsure sowie den Vitaminen C und E bei und schtzt die Zelle vor einer Kettenreaktion, die Zellschden verursachen kann

10.3390/cancers15184525 119 ShihY

Ocitinib-resistant cells can enhance glucose and Gln uptake, while inhibiting Gln uptake and metabolism in NSCLC, effectively reducing the proliferation of ocitinib resistant cells and promoting cell apoptosis (27)