Re-thinking cell cycle regulators: the cross-talk with metabolism.
Details
State: Public
Version: author
Serval ID
serval:BIB_921481056DE6
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Re-thinking cell cycle regulators: the cross-talk with metabolism.
Journal
Frontiers In Oncology
ISSN
2234-943X (Electronic)
ISSN-L
2234-943X
Publication state
Published
Issued date
2013
Volume
3
Pages
4
Language
english
Notes
Publication types: Journal Article
Publication Status: epublish
Publication Status: epublish
Abstract
Analysis of genetically engineered mice deficient in cell cycle regulators, including E2F1, cdk4, and pRB, showed that the major phenotypes are metabolic perturbations. These key cell cycle regulators contribute to lipid synthesis, glucose production, insulin secretion, and glycolytic metabolism. It has been shown that deregulation of these pathways can lead to metabolic perturbations and related metabolic diseases, such as obesity and type II diabetes. The cyclin-cdk-Rb-E2F1 pathway regulates adipogenesis in addition to its well-described roles in cell cycle regulation and cancer. It was also shown that E2F1 directly participates in the regulation of pancreatic growth and function. Similarly, cyclin D3, cdk4, and cdk9 are also adipogenic factors with strong effects on whole organism metabolism. These examples support the emerging notion that cell cycle regulatory proteins also modulate metabolic processes. These cell cycle regulators are activated by insulin and glucose, even in non-proliferating cells. Most importantly, these cell cycle regulators trigger the adaptive metabolic switch that normal and cancer cells require in order to proliferate. These changes include increased lipid synthesis, decreased oxidative metabolism, and increased glycolytic metabolism. In summary, these factors are essential regulators of anabolic biosynthetic processes, blocking at the same time oxidative and catabolic pathways, which is reminiscent of cancer cell metabolism.
Pubmed
Open Access
Yes
Create date
07/03/2013 16:40
Last modification date
20/08/2019 15:55