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Updated: Apr 12, 2026

Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells
Published on: June 9, 2020
Gemcitabine Induces Radiosensitization Through Inhibition of RAD51-dependent Repair for DNA Double-strand Breaks
Shinko Kobashigawa1, Keiko Morikawa2, Hiromu Mori1
1Department of Radiology, School of Medicine, Oita University, Oita, Japan.
Background/Aim:
Gemcitabine (GEM) is used in clinical chemo-radiotherapy; however, the mechanism that contributes to enhanced radiosensitivity by GEM is not fully-understood. We evaluated the effect of GEM on radiosensitization in pancreatic cancer cell lines.
Materials And Methods:
Pancreatic cell lines PK-59 and PK-45p were used. A total of 5 μM GEM for 4 h were administered pre- or post-gamma irradiation.
Results:
Enhanced cell killing effects by GEM in radiotherapy were observed for pre-treatment but not post-treatment GEM. We focused on the dynamics of RAD51 and phospho-H2AX foci after irradiation. Significantly higher numbers of phospho-H2AX foci were observed in GEM pre-treated cells than in untreated cells after irradiation. We also found inhibition of the formation and degradation of RAD51 foci by GEM pre-treatment. The radiosensitizing effect of GEM was suppressed by knockdown of RAD51.
Conclusion:
RAD51-dependent homologous recombination is one of the key targets in the GEM-induced radiosensitizing effect.
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