Epigenetic Marks Repressing Gluconeogenesis in Liver and Kidney Cancer.
editorial · Level V
Where this comes from
- Record sourced from PubMed, PMID 32060227.
- Also identified by DOI 10.1158/0008-5472.CAN-19-3953.
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Abstract
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 <i>Cancer Research</i>, 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.<i>See related article by Liao et al., p. 675</i>.
Medical subject headings
- Gluconeogenesis
- Kidney Neoplasms