期刊
CANCER RESEARCH
卷 80, 期 4, 页码 657-658出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-19-3953
关键词
-
类别
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据