In vitro study demonstrates that arabinoside cytosine increases proton-induced DNA double-strand breaks in melanoma cells, highlighting a mechanism to enhance radiosensitivity.
Increasing the radiosensitivity of normal and tumor cells is one of the priority aims of modern radiobiology. The agents that modify the yield of DNA double-strand breaks (DSBs) which are lethal to cells are of particular interest. We have previously shown that under the influence of DNA repair inhibitor - arabinosid cytosine (AraC) the DNA DSBs yield on cells of various types increases under the action of ionizing radiation. The mechanism of this process is based on the long-term non-reparable DNA single-strand breaks (SSBs) conversion into enzymatic DSBs. The main aim of this research was to elucidate the molecular and cellular effects of the proton action on the murine melanoma B16 cells under the influence of AraC. It was found that the amount of DNA SSB and DSB significantly increases under the influence of AraC. This difference persists in the post-radiation period up to 9 days.
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Kozhina et al. (2022) studied this question.
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