期刊
CELL CYCLE
卷 15, 期 17, 页码 2248-2255出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2016.1207840
关键词
bistability; LATS; mutant p53; RNF20; SREBP; statins; YAP
类别
资金
- Israel Science Foundation [1779/21]
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
- European Research Council [293438]
- Robert Bosch Stiftung [12.5.8000.0094.2]
- German-Israeli Foundation (GIF)
- Moross Integrated Cancer Center
- European Research Council (ERC) [293438] Funding Source: European Research Council (ERC)
Increased rates of cholesterol and lipid synthesis have long been recognized as important aspects of the metabolic rewiring that occurs during cancerous transformation. Many genes encoding enzymes involved in cholesterol and fatty acid biogenesis are transcriptional targets of the sterol regulatory element-binding proteins (SREBPs). The SREBPs act as a hub for metabolic and proliferation-related signals; their activity is the focus of a tug-of-war between tumor suppressors, who generally inhibit SREBP function, and oncogenes, who often promote, and rely on, SREBP activity. The Hippo pathway plays a central role in coordinating cell proliferation and organ size, whereas p53 is a crucial tumor suppressor that maintains metabolic homeostasis and orchestrates cellular stress responses. Together, the Hippo and p53 signaling pathways cooperate on multiple levels to fine-tune SREPB activity and regulate cholesterol/lipid levels. Cholesterol biosynthesis inhibitors such as statins are appealing conceptually, but have yet to show an indisputable effect on cancer development. Fortunately, the complex regulation surrounding the Hippo-p53-SREBP network potentially provides a broad interface for additional novel cancer-targeting interventions.
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