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Related Concept Videos

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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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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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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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Related Experiment Video

Updated: Aug 19, 2025

Monitoring of Ubiquitin-proteasome Activity in Living Cells Using a Degron dgn-destabilized Green Fluorescent Protein GFP-based Reporter Protein
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IGF-1 Accelerates Cell Aging by Inhibiting POLD1 Expression.

Yu Li Hou1, Yi Fei Wang2, Qiao Song1

  • 1Department of Clinical Laboratory, Xuanwu Hospital, National Clinical Research Center for Geriatric Diseases, Capital Medical University, Beijing 100053, China.

Biomedical and Environmental Sciences : BES
|November 28, 2022
PubMed
Summary

Insulin-like growth factor-1 (IGF-1) promotes cell aging by inhibiting DNA polymerase delta 1 (POLD1) expression. Restoring POLD1 levels can reverse IGF-1-induced aging, offering new anti-aging therapeutic targets.

Keywords:
AgingDNA polymerase delta 1Insulin-like growth factor-1Linsitinib

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Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Aging Research

Background:

  • The precise mechanisms of aging and the insulin-like growth factor-1 (IGF-1) signaling pathway remain incompletely understood.
  • Investigating the role of DNA polymerase delta 1 (POLD1) in cellular aging is crucial for understanding age-related molecular changes.

Purpose of the Study:

  • To explore the effect of POLD1 on the IGF-1 signaling pathway in the context of cell aging.
  • To elucidate the molecular interplay between IGF-1, POLD1, and cellular senescence.

Main Methods:

  • Analysis of IGF-1 and POLD1 expression in aging human serum and mouse tissues.
  • Incubation of 2BS cells with human serum, IGF-1 protein, or linsitinib to assess effects on POLD1 expression and senescence.
  • Manipulation of POLD1 expression (overexpression and knockdown) to determine its role in IGF-1-mediated aging.

Main Results:

  • IGF-1 expression increased, while POLD1 expression decreased with aging.
  • Old-age serum and IGF-1 treatment induced senescence and reduced POLD1 levels, effects reversible by linsitinib or POLD1 overexpression.
  • Linsitinib's anti-aging effect was abrogated by POLD1 knockdown, confirming POLD1's critical role.

Conclusions:

  • IGF-1 promotes aging by inhibiting POLD1 expression via IGF-1R.
  • POLD1 acts as a key mediator in the IGF-1 signaling pathway's effect on cellular aging.
  • Targeting the IGF-1/POLD1 axis presents a novel strategy for anti-aging interventions.