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Related Concept Videos

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Abnormal Proliferation

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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P2Y12 Receptor Antagonists Decrease the Radiation Resistance of B16 Melanoma by Suppressing DNA Repair.

Yuma Mizoguchi1, Natsuki Mori1, Kazuki Kitabatake1

  • 1Department of Radiation Biosciences, Faculty of Pharmaceutical Sciences, Tokyo University of Science, 6-3-1 Niijuku, Katsushika-ku, Tokyo 125-8585, Japan.

Biological & Pharmaceutical Bulletin
|November 19, 2025
PubMed
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P2Y12 receptor antagonists can enhance radiation therapy by inhibiting cancer cell DNA repair. This suppression of the DNA damage response (DDR) increases cancer cell death and improves antitumor effects, suggesting their potential as radiosensitizers.

Keywords:
DNA damage responseP2Y12 receptorcancerradiation therapysublethal damage recovery

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Area of Science:

  • Oncology
  • Molecular Biology
  • Radiotherapy

Background:

  • Cancer cells repair DNA double-strand breaks (DSBs) induced by radiation, leading to radioresistance.
  • Suppressing DNA repair mechanisms offers a strategy to enhance radiation therapy's efficacy.

Purpose of the Study:

  • To investigate the role of the P2Y12 receptor in radioresistance of mouse B16 melanoma cells.
  • To evaluate P2Y12 receptor antagonists as potential radiosensitizers.

Main Methods:

  • In vitro and in vivo experiments using mouse B16 melanoma cells.
  • Treatment with P2Y12 receptor antagonists (Clopidogrel, PSB0739) and agonist (ADP).
  • Assessment of DNA damage response (DDR), unrepaired DNA sites, and cell death after gamma irradiation.
  • P2Y12 receptor knockdown and evaluation of fractionated irradiation effects.

Main Results:

  • P2Y12 receptor antagonists suppressed DDR, increased unrepaired DNA, and enhanced radiation-induced cell death in B16 melanoma cells.
  • ADP (P2Y12 agonist) increased radioresistance by enhancing DDR.
  • P2Y12 receptor knockdown increased unrepaired DNA and cell death after irradiation.
  • P2Y12 suppression enhanced the efficacy of fractionated irradiation and in vivo antitumor effects of gamma irradiation.

Conclusions:

  • The P2Y12 receptor plays a significant role in melanoma radioresistance.
  • P2Y12 receptor antagonists demonstrate radiosensitizing effects by inhibiting DNA repair.
  • P2Y12 receptor antagonists are promising agents for improving radiation therapy outcomes.