Abstract
In the past years, several lines of evidence have shown that cell cycle regulatory proteins also can modulate metabolic processes. The transcription factor E2F1 is a central player involved in cell cycle progression, DNA-damage response, and apoptosis. Its crucial role in the control of cell fate has been extensively studied and reviewed before; however, here, we focus on the participation of E2F1 in the regulation of metabolism. We summarize recent findings about the cell cycle-independent roles of E2F1 in various tissues that contribute to global metabolic homeostasis and highlight that E2F1 activity is increased during obesity. Finally, coming back to the pivotal role of E2F1 in cancer development, we discuss how E2F1 links cell cycle progression with different metabolic adaptations required for cell growth and survival.
Highlights
A CELL CYCLE PROTEIN WITH NEW SKILLSThe E2F transcription factors were first identified as proteins that were able to bind to the promoter of the adenoviral gene E2 [1]
We have collected the current and emerging evidence showing that E2F1 regulates metabolism in non-proliferating conditions and, more importantly, that dysregulation of E2F1 activity leads to complications associated with obesity
Many studies have focused on the mitogenic signals that drive E2F1 activation in cancer cells, but how E2F1 is activated in other pathological conditions such as obesity is just beginning to be understood
Summary
A CELL CYCLE PROTEIN WITH NEW SKILLSThe E2F transcription factors were first identified as proteins that were able to bind to the promoter of the adenoviral gene E2 [1]. We summarize recent findings about the cell cycle-independent roles of E2F1 in various tissues that contribute to global metabolic homeostasis and highlight that E2F1 activity is increased during obesity. Chromatin immunoprecipitation (ChIP) analysis revealed that in basal conditions E2F1 and pRB form a repressor complex in the promoters of several genes involved in oxidative metabolism and mitochondrial biogenesis in muscle, and in brown adipose tissue [34].
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