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Related Experiment Videos

Delay in entry into S phase after heat shock.

D L Dewey, J L Holden

    Cell and Tissue Kinetics
    |July 1, 1984
    PubMed
    Summary
    This summary is machine-generated.

    Heat shock delays DNA synthesis in melanoma cells, particularly when applied at the G1 phase. This G1 phase also shows resistance to hyperthermic cell killing and impacts subsequent DNA replication.

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    Area of Science:

    • Cell Biology
    • Cancer Research
    • Hyperthermia Treatment

    Background:

    • Hyperthermia (heat shock) is explored as a potential cancer therapy.
    • Understanding cell cycle responses to heat shock is crucial for optimizing treatment efficacy.
    • The Harding Passey melanoma cell line provides a model for studying heat shock effects.

    Purpose of the Study:

    • To investigate the impact of heat shock on cell cycle progression in synchronized melanoma cells.
    • To determine the specific timing of heat shock's effect on DNA synthesis (S phase).
    • To assess the relationship between heat shock timing, cell cycle phase, and cellular resistance.

    Main Methods:

    • Synchronized Harding Passey melanoma cells were subjected to a controlled heat shock (44°C for 36 min).

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  • Thymidine incorporation was measured at regular intervals post-heat shock to monitor DNA synthesis onset.
  • Cellular resistance to hyperthermic killing and thymidine incorporation were evaluated across different cell cycle phases.

    • Main Results:

    • Heat shock applied at the end of the G1 phase delayed the subsequent S phase by 20 hours.
    • Heat shock at other cell cycle stages resulted in even longer delays before S phase onset.
    • The G1 phase exhibited the highest resistance to hyperthermic killing and showed the least impact on subsequent thymidine incorporation.

    Conclusions:

    • The timing of heat shock is critical in determining its effect on melanoma cell cycle progression.
    • The G1 phase is a key period of resistance to hyperthermia, both in terms of cell killing and DNA synthesis disruption.
    • Thermotolerance, observed in heat shock killing, also extends to the delay of cell cycle progression.