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2016 ; 15
(17
): 2248-55
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The Hippo pathway, p53 and cholesterol
#MMPMID27419353
Aylon Y
; Oren M
Cell Cycle
2016[Sep]; 15
(17
): 2248-55
PMID27419353
show ga
ASBTRACT 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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