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Fig. 2 | Experimental Hematology & Oncology

Fig. 2

From: The metabolic adaptation mechanism of metastatic organotropism

Fig. 2

Metabolic adaptation mechanism of metastatic organotropism. Cancers that metastasize to bone (a), liver (b), lung (c) and brain (d), omentum, and lymph nodes need to adapt to different metabolic microenvironments to survive and grow at a distant site. Metastasizing cancer cells need to adapt to the metabolic microenvironments of the secondary organ, which mainly includes changes in energy and nutrient sources, organ-specific metabolites, pH, the degree of hypoxia, and the metabolic interactions between organ-specific cells and cancer cells. HA hydroxyapatite, Ser serine, Lact lactate, FA fatty acid, BMSCs bone marrow stromal cells, ALDOB aldolase B, HSCs hepatic stellate cells; HMFs hepatic myofibroblasts, OXPHOS oxidative phosphorylation, CKB brain-type creatine kinase, FAO fatty acid oxidation, PGC-1α peroxisome proliferation-activated receptor co-activator 1 alpha; PRDX2 peroxiredoxin-2, PRODH proline dehydrogenase, ASNS asparagine synthetase, PC pyruvate carboxylase, ALT alanine aminotransferase, α-KG α-ketoglutarate, ECM extracellular matrix, GABA gamma-aminobutyrate, PPP pentose phosphate pathway, Glu glutamate, BCAA branched chain amino acid

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