Journal Article

Acquisition of radioresistance by IL-6 treatment is caused by suppression of oxidative stress derived from mitochondria after γ-irradiation

Yuki Tamari, Genro Kashino and Hiromu Mori

in Journal of Radiation Research

Volume 58, issue 4, pages 412-420
Published in print July 2017 | ISSN: 0449-3060
Published online February 2017 | e-ISSN: 1349-9157 | DOI: http://dx.doi.org/10.1093/jrr/rrw084
Acquisition of radioresistance by IL-6 treatment is caused by suppression of oxidative stress derived from mitochondria after γ-irradiation

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  • Clinical Genetics
  • Molecular Biology and Genetics
  • Epidemiology
  • Radiology
  • Nuclear Chemistry, Photochemistry, and Radiation

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Abstract

Interleukin (IL)-6 is a multifunctional cytokine and is one of the radiation-induced bystander factors. This study aimed to clarify the mechanism of acquisition of radioresistance through the control of reactive oxygen species (ROS) by IL-6. We used a rat glioma cell line (C6) as tumor cells and a rat astrocyte cell line (RNB) as non-tumor cells. Our results showed that the surviving fraction of C6 cells after 6 Gy irradiation was increased by the addition of IL-6, but that this was not the case in RNB cells. In addition, the number of 53BP1 foci in C6 cells at 30 min after γ-irradiation were decreased by IL-6. Levels of ROS in whole C6 cells, and superoxide in the mitochondria of C6 cells immediately after γ-irradiation, were reduced by IL-6, but this was not observed in RNB cells. The mitochondrial membrane potential detected by JC-1 in C6 and RNB cells was inhibited by IL-6 alone. Therefore, it was concluded that IL-6 leads specifically to radioresistance in tumor cells by inhibition of increases in ROS after γ-irradiation.

Keywords: IL-6; radioresistance; ROS; mitochondria

Journal Article.  4631 words.  Illustrated.

Subjects: Clinical Genetics ; Molecular Biology and Genetics ; Epidemiology ; Radiology ; Nuclear Chemistry, Photochemistry, and Radiation

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