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Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
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To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
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The cell cycle regulation directs how a cell proceeds from one phase to the next and begins mitosis. The cell cycle control system includes intracellular regulatory molecules and external triggers. They provide "stop" or "advance" signals and operate at specific cell cycle stages termed checkpoints to ensure that a particular process is completed before the cell advances to the next phase.
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The cell cycle is an organized set of events that leads the cell to divide into two daughter cells, each containing chromosomes identical to the parent cell. It is the cell cycle that leads to the formation of an entire organism from a single-cell zygote. Besides, cell division also functions in the renewal or repair of tissues in adult multicellular eukaryotes. For example, in the bone marrow, the stem cells divide to form new blood cells. Although essential for several functions, cell...
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CDH1 Orchestrates Anabolic Events to Promote Cell Cycle Initiation.

Yun-Zi Mao1, Jiao-Jiao Zhang1,2, Meng-Qi You1

  • 1The Obstetrics and Gynecology Hospital of Fudan University, Shanghai Key Lab of Reproduction and Development, Shanghai Key Lab of Female Reproductive Endocrine Related Diseases, Shanghai Key Laboratory of Metabolic Remodeling and Health, State Key Laboratory of Genetics and Development of Complex Phenotypes, and Institutes of Biomedical Sciences, Fudan Unviersity, Shanghai, 200433, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|September 29, 2025
PubMed
Summary
This summary is machine-generated.

The cell cycle regulator CDH1 coordinates cell growth by managing anabolism, activating HIF1α for metabolism and AARS2 to conserve resources, thus promoting cell proliferation and cancer progression.

Keywords:
CDH1R5Panabolismcell cycle

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Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1
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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Cell proliferation necessitates anabolic processes, but the integration of anabolism with the cell cycle remains unclear.
  • Understanding how cells initiate proliferation requires investigating the coordination of metabolic pathways with cell cycle progression.

Purpose of the Study:

  • To elucidate the role of the G1-phase regulator CDH1 in coordinating anabolic events for cell cycle initiation.
  • To identify the molecular mechanisms by which CDH1 influences metabolism and anabolite levels during cell cycle progression.

Main Methods:

  • Investigated the degradation of Von Hippel-Lindau (VHL) by CDH1.
  • Analyzed the activation of hypoxia-inducible factor 1α (HIF1α) and alanyl tRNA synthetase (AARS2) by CDH1.
  • Examined the interaction of ribose-5-phosphate (R5P) with transketolase-like-1 (TKTL1) and its role in CDH1 regulation.

Main Results:

  • CDH1 degrades VHL, activating HIF1α for enhanced glucose metabolism and angiogenesis.
  • CDH1 activates AARS2, leading to the inactivation of pyruvate dehydrogenase E1 subunit alpha 1 (PDHA1) and anabolite conservation.
  • R5P, accumulated due to CDH1 activity, binds TKTL1, bridging CDH1 to CDK2 and SCFβ-TRCP for CDH1 phosphorylation and degradation, promoting cell cycle initiation.
  • Low R5P and high CDH1 expression correlate with cancer cell proliferation.
  • Artificial R5P (R5S) induces apoptosis in cancer cells by initiating the cell cycle without sufficient anabolites.

Conclusions:

  • CDH1 acts as a central coordinator of anabolism to ensure cell cycle initiation.
  • The identified CDH1-VHL-HIF1α/AARS2-R5P/TKTL1 circuit is crucial for cell proliferation and is implicated in cancer signatures like the Warburg effect and angiogenesis.
  • Targeting this circuit offers potential therapeutic strategies for cancer treatment.