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    Gluconeogenesis is frequently suppressed in tumors arising in gluconeogenic organs and reexpression of a gluconeogenesis enzyme, fructose-1,6-bisphosphatase (FBP1), was found to inhibit tumor growth. In this issue of Cancer Research, Liao and colleagues show that histone H3 trimethylation on lysine 27, induced by polycomb repressive complex 2 (PRC2), is responsible for downregulating FBP1 in liver and kidney cancer cells. Moreover, they identified FBP1 repression as an important downstream mechanism of PRC2-mediated carcinogenesis. FBP1 inhibits glycolysis but also directly interferes with PRC2 function, thus FBP1 and PRC2 are part of a novel negative feedback loop that is deregulated in liver and kidney cancer.See related article by Liao et al., p. 675. ©2020 American Association for Cancer Research.


    Katharina Leithner. Epigenetic Marks Repressing Gluconeogenesis in Liver and Kidney Cancer. Cancer research. 2020 Feb 15;80(4):657-658

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    PMID: 32060227

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