Gemcitabine is used in clinical chemo-radiotherapy; however, the mechanism underlying enhanced radiosensitivity by gemcitabine is not fully elucidated. We evaluated the role of gemcitabine in mammalian cell lines using a therapeutic high energy 10 MeV linac-X-ray irradiation device. Rodent cell lines CHO and xrs5 were used. A total of 5 μM gemcitabine for 24 hours was administered with or without post-X-ray irradiation. DNA double-strand breaks (DSBs) and cell enlargement were observed by using singly gemcitabine. Enhanced cell killing effects by radiotherapy were observed with gemcitabine pre-treatment in both CHO and xrs5 cells. We focused on the dynamics of phosphorylated p53-binding protein 1 (53BP1)-positive foci after irradiation. Significantly higher numbers of 53BP1 foci were observed after irradiation in gemcitabine pre-treated cells than in untreated cells. The radiosensitizing effect of gemcitabine was not suppressed in the non-homologous end joining (NHEJ) deficient xrs5 cells. We confirmed that in rodent cells the radiosensitizing effect of gemcitabine is related to suppression of a repair pathway other than NHEJ.
| Published in | American Journal of Laboratory Medicine (Volume 2, Issue 6) |
| DOI | 10.11648/j.ajlm.20170206.15 |
| Page(s) | 137-143 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2017. Published by Science Publishing Group |
Radiosensitization, Gemcitabine, Non-homologous End Joining, 53BP1
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APA Style
Keiko Morikawa, Yoshida Yukito, Yuh Sugii, Genro Kashino, Hiromu Mori. (2017). The Effect of Radiosensitization of Gemcitabine Related to Suppression of a Repair Pathway: Examination of Mammalian Cells with Therapeutic High Energy X-rays. American Journal of Laboratory Medicine, 2(6), 137-143. https://doi.org/10.11648/j.ajlm.20170206.15
ACS Style
Keiko Morikawa; Yoshida Yukito; Yuh Sugii; Genro Kashino; Hiromu Mori. The Effect of Radiosensitization of Gemcitabine Related to Suppression of a Repair Pathway: Examination of Mammalian Cells with Therapeutic High Energy X-rays. Am. J. Lab. Med. 2017, 2(6), 137-143. doi: 10.11648/j.ajlm.20170206.15
AMA Style
Keiko Morikawa, Yoshida Yukito, Yuh Sugii, Genro Kashino, Hiromu Mori. The Effect of Radiosensitization of Gemcitabine Related to Suppression of a Repair Pathway: Examination of Mammalian Cells with Therapeutic High Energy X-rays. Am J Lab Med. 2017;2(6):137-143. doi: 10.11648/j.ajlm.20170206.15
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Download@article{10.11648/j.ajlm.20170206.15,
author = {Keiko Morikawa and Yoshida Yukito and Yuh Sugii and Genro Kashino and Hiromu Mori},
title = {The Effect of Radiosensitization of Gemcitabine Related to Suppression of a Repair Pathway: Examination of Mammalian Cells with Therapeutic High Energy X-rays},
journal = {American Journal of Laboratory Medicine},
volume = {2},
number = {6},
pages = {137-143},
doi = {10.11648/j.ajlm.20170206.15},
url = {https://doi.org/10.11648/j.ajlm.20170206.15},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajlm.20170206.15},
abstract = {Gemcitabine is used in clinical chemo-radiotherapy; however, the mechanism underlying enhanced radiosensitivity by gemcitabine is not fully elucidated. We evaluated the role of gemcitabine in mammalian cell lines using a therapeutic high energy 10 MeV linac-X-ray irradiation device. Rodent cell lines CHO and xrs5 were used. A total of 5 μM gemcitabine for 24 hours was administered with or without post-X-ray irradiation. DNA double-strand breaks (DSBs) and cell enlargement were observed by using singly gemcitabine. Enhanced cell killing effects by radiotherapy were observed with gemcitabine pre-treatment in both CHO and xrs5 cells. We focused on the dynamics of phosphorylated p53-binding protein 1 (53BP1)-positive foci after irradiation. Significantly higher numbers of 53BP1 foci were observed after irradiation in gemcitabine pre-treated cells than in untreated cells. The radiosensitizing effect of gemcitabine was not suppressed in the non-homologous end joining (NHEJ) deficient xrs5 cells. We confirmed that in rodent cells the radiosensitizing effect of gemcitabine is related to suppression of a repair pathway other than NHEJ.},
year = {2017}
}
TY - JOUR T1 - The Effect of Radiosensitization of Gemcitabine Related to Suppression of a Repair Pathway: Examination of Mammalian Cells with Therapeutic High Energy X-rays AU - Keiko Morikawa AU - Yoshida Yukito AU - Yuh Sugii AU - Genro Kashino AU - Hiromu Mori Y1 - 2017/11/07 PY - 2017 N1 - https://doi.org/10.11648/j.ajlm.20170206.15 DO - 10.11648/j.ajlm.20170206.15 T2 - American Journal of Laboratory Medicine JF - American Journal of Laboratory Medicine JO - American Journal of Laboratory Medicine SP - 137 EP - 143 PB - Science Publishing Group SN - 2575-386X UR - https://doi.org/10.11648/j.ajlm.20170206.15 AB - Gemcitabine is used in clinical chemo-radiotherapy; however, the mechanism underlying enhanced radiosensitivity by gemcitabine is not fully elucidated. We evaluated the role of gemcitabine in mammalian cell lines using a therapeutic high energy 10 MeV linac-X-ray irradiation device. Rodent cell lines CHO and xrs5 were used. A total of 5 μM gemcitabine for 24 hours was administered with or without post-X-ray irradiation. DNA double-strand breaks (DSBs) and cell enlargement were observed by using singly gemcitabine. Enhanced cell killing effects by radiotherapy were observed with gemcitabine pre-treatment in both CHO and xrs5 cells. We focused on the dynamics of phosphorylated p53-binding protein 1 (53BP1)-positive foci after irradiation. Significantly higher numbers of 53BP1 foci were observed after irradiation in gemcitabine pre-treated cells than in untreated cells. The radiosensitizing effect of gemcitabine was not suppressed in the non-homologous end joining (NHEJ) deficient xrs5 cells. We confirmed that in rodent cells the radiosensitizing effect of gemcitabine is related to suppression of a repair pathway other than NHEJ. VL - 2 IS - 6 ER -
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