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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

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 the telomeric...
Replicative Cell Senescence02:15

Replicative Cell Senescence

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 the telomeric...
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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fulfill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.
Many Proteins Orchestrate Replication at the Origin
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Replication in Eukaryotes02:31

Replication in Eukaryotes

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Related Experiment Video

Updated: Jul 5, 2026

Studying Age-dependent Genomic Instability using the S. cerevisiae Chronological Lifespan Model
08:46

Studying Age-dependent Genomic Instability using the S. cerevisiae Chronological Lifespan Model

Published on: September 29, 2011

Cellular life span and the Warburg effect.

Hiroshi Kondoh1

  • 1Department of Geriatric Medicine, Graduate School of Medicine, Kyoto University, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto, 606-8507, Japan. hkondoh@kuhp.kyoto-u.ac.jp

Experimental Cell Research
|April 16, 2008
PubMed
Summary

Most cancers exhibit enhanced glycolysis, known as the Warburg effect. This metabolic shift is crucial for early tumor development, aiding cell immortalization and adaptation to low-oxygen environments.

Area of Science:

  • Cellular metabolism
  • Cancer biology
  • Senescence

Background:

  • The Warburg effect, enhanced glycolysis in cancer cells, is a hallmark of most cancers.
  • Senescent cells also exhibit metabolic shifts, suggesting a role in early tumorigenesis.
  • Understanding this metabolic reprogramming is key to cancer research.

Purpose of the Study:

  • To investigate the role of enhanced glycolysis in early tumorigenesis.
  • To explore the link between senescence and metabolic shifts in cancer development.
  • To identify novel regulatory mechanisms of this metabolic reprogramming.

Main Methods:

  • Comparative analysis of metabolic profiles in immortalized, senescent, and cancerous cells.
  • Investigation of glycolysis and mitochondrial respiration pathways.

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  • Exploration of regulatory mechanisms underlying metabolic shifts.
  • Main Results:

    • Confirmed enhanced glycolysis and reduced mitochondrial respiration in immortalized, senescent, and cancerous cells.
    • Identified a common metabolic shift across these cell types.
    • Highlighted the poorly characterized nature of the underlying regulatory mechanisms.

    Conclusions:

    • Enhanced glycolysis is a critical metabolic adaptation during early tumorigenesis.
    • The metabolic shift observed in senescent cells mirrors that in cancer cells.
    • Discovering novel regulatory mechanisms is essential for future cancer diagnostics and therapeutics.