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Cancer metabolism refers to the alterations in cellular metabolism pathways that are evident in cancer cells compared with most normal tissue cells. Metabolic alterations in cancer cells are numerous and include aerobic glycolysis, reduced oxidative phosphorylation and the increased generation of biosynthetic intermediates needed for cell growth and proliferation.
The mechanisms that drive cancer cachexia are unclear. Adipocyte activation of GPR81 by high levels of lactate is now shown to drive adipose tissue browning, thermogenesis and a loss of body weight in mouse models of cancer.
Two independent studies published in Nature implicate distal cholesterol biosynthesis in the regulation of ferroptosis and show that 7-dehydrocholesterol (7-DHC) is an endogenous, anti-ferroptotic metabolite.
The tumour microenvironment produces nutrients that propel cancer development. New work finds that pancreatic ductal adenocarcinoma cells use one such nutrient, acetate, to alter protein acetylation, rerouting polyamine metabolism and promoting cell growth under acidosis—a finding with potential implications for treating this cancer.
The chemoresistant and immunoevasive characteristics of leukaemia stem cells (LSCs) impede the treatment efficacy for acute myeloid leukaemia (AML). We find that inhibiting the tyrosine phosphatase SHP-1 effectively alters the metabolic state of LSCs, making them more susceptible to chemotherapy and immune surveillance in AML.