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Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
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Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
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Mitotic progression following DNA damage enables pattern recognition within micronuclei.

Shane M Harding1, Joseph L Benci2,3,4, Jerome Irianto5,6,7

  • 1Department of Cancer Biology, Basser Center for BRCA, Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, 421 Curie Boulevard, Philadelphia, Pennsylvania 19104, USA.

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Genotoxic cancer therapy triggers delayed inflammation via cell cycle progression into mitosis, leading to micronuclei formation. This process is crucial for abscopal tumor responses when combined with radiation and immune checkpoint blockade.

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Area of Science:

  • Oncology
  • Immunology
  • Cell Biology

Background:

  • Genotoxic cancer therapies induce inflammatory gene expression, but the underlying mechanisms and delayed onset are poorly understood.
  • Inflammatory cytokines are vital for local and abscopal tumor responses to radiotherapy by modulating the tumor microenvironment.
  • The delayed inflammatory response (days) contrasts with acute DNA-damage responses (minutes to hours), suggesting additional rate-limiting steps.

Purpose of the Study:

  • To elucidate the mechanisms driving DNA-damage-induced inflammation following genotoxic cancer therapy.
  • To investigate the role of cell cycle progression and micronuclei formation in inflammatory signaling.
  • To assess the impact of STING-cGAS pathway and cell cycle modulation on abscopal tumor regression in vivo.

Main Methods:

  • Investigated the link between double-stranded DNA breaks, cell cycle progression through mitosis, and micronuclei formation.
  • Assessed the role of cyclic GMP-AMP synthase (cGAS) within micronuclei in activating inflammatory signaling.
  • Utilized STING-cGAS pathway inhibition and cell cycle progression blockade in cellular and in vivo models.

Main Results:

  • Cell cycle progression through mitosis post-DNA breaks leads to micronuclei formation, preceding inflammatory signaling activation.
  • Micronuclei serve as repositories for cGAS, a pattern-recognition receptor crucial for interferon signaling.
  • Inhibition of mitosis or STING-cGAS pathway impaired interferon signaling; STING loss prevented abscopal tumor regression in vivo.

Conclusions:

  • Temporal modulation of the cell cycle, specifically progression through mitosis and subsequent micronuclei formation, is a critical rate-limiting step for DNA-damage-induced inflammation.
  • The STING-cGAS pathway activated by micronuclei is essential for abscopal tumor responses to radiotherapy combined with immune checkpoint blockade.
  • Targeting cell cycle progression may enhance therapeutic strategies combining genotoxic agents with immune checkpoint inhibitors.