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Related Concept Videos

Replicative Cell Senescence02:15

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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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Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012...
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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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Techniques to Induce and Quantify Cellular Senescence
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Bypassing senescence.

Annalisa M VanHook1

  • 1Science Signaling, AAAS, Washington, DC 20005, USA.

Science Signaling
|January 21, 2025
PubMed
Summary

Liver cells in damaged livers can switch their metabolism to avoid aging and develop into tumors. This metabolic switch is key to tumor formation in liver disease.

Area of Science:

  • Hepatocyte biology
  • Cancer research
  • Metabolic regulation

Background:

  • Liver damage can lead to cellular senescence, a state of irreversible growth arrest.
  • Senescent cells can promote inflammation and tissue dysfunction.
  • Tumor formation in damaged livers is a significant clinical challenge.

Purpose of the Study:

  • To investigate the role of metabolic changes in hepatocyte senescence escape.
  • To understand how senescent hepatocytes contribute to tumor development.
  • To identify potential therapeutic targets for liver cancer.

Main Methods:

  • Analysis of metabolic pathways in senescent and non-senescent hepatocytes.
  • In vivo and in vitro models of liver damage and tumor formation.

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  • Genetic and pharmacological manipulation of metabolic processes.

    • Main Results:

    • A specific metabolic switch was identified in hepatocytes that allows them to bypass senescence.
    • This metabolic reprogramming is crucial for the proliferation of damaged hepatocytes.
    • Targeting this metabolic switch inhibited tumor formation in preclinical models.

    Conclusions:

    • Metabolic plasticity is a critical factor enabling damaged hepatocytes to evade senescence and initiate tumorigenesis.
    • The identified metabolic switch represents a potential therapeutic vulnerability in liver cancer.
    • Understanding hepatocyte metabolism is essential for developing strategies against liver disease progression and cancer.