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Fig. 3 | Molecular Cancer

Fig. 3

From: The critical roles of activated stellate cells-mediated paracrine signaling, metabolism and onco-immunology in pancreatic ductal adenocarcinoma

Fig. 3

PSCs in metabolic reprogramming. In KRAS-dependent pathways, diverse cytokines and signaling pathways mediate metabolic interactions between PSCs and PDA cells. KRAS-driven glutamine (Gln) metabolism becomes a major carbon source for tumor cells survival; PSCs-derived IGF elevates mitochondrial respiration in PDA cells via IGF1R/AXL axis; KRAS-mutant PDA cells can obtain extracellular proteins for supporting growth through upregulated macropinocytosis. PSCs-secreted non-essential amino acids (NEAAs), such as autophagy-induced Ala, can serve as an alternative energy source to fuel PDA cells. In KRAS-independent pathways, PSCs-derived growth factors (GFs) and exosomes play a pivotal role in mediating survival, proliferation, metastasis, biosynthesis of tumor cells

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