Telomere-Mitochondrion Links Contribute to Induction of Senescence in MCF-7 Cells after Carbon-Ion Irradiation

Miao, Guo-Ying; Zhou, Xin; Zhang, Xin; Xie, Yi; Sun, Chao; Liu, Yang; Gan, Lu; Zhang, Hong

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자료유형: 학술저널

저자정보: Miao, Guo-Ying (Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences) Zhou, Xin (Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences) Zhang, Xin (Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences) Xie, Yi (Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences) Sun, Chao (Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences) Liu, Yang (Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences) Gan, Lu (Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences) Zhang, Hong (Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences)

저널정보: 아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제17권 제4호

발행연도: 2016.1

수록면: 1,993 - 1,998 (6page)

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The effects of carbon-ion irradiation on cancer cell telomere function have not been comprehensively studied. In our previous report cancer cells with telomere dysfunction were more sensitive to carbon-ion irradiation, but the underlying mechanisms remained unclear. Here we found that telomerase activity was suppressed by carbon-ion irradiation via hTERT down-regulation. Inhibition of telomere activity by MST-312 further increased cancer cell radiosensitivity to carbon-ion radiation. hTERT suppression caused by either carbon-ion irradiation or MST-312 impaired mitochondrial function, as indicated by decreased membrane potential, mtDNA copy number, mitochondrial mass, total ATP levels and elevated reactive oxygen species (ROS). PGC-$1{\alpha}$ expression was repressed after carbion-ion irradiation, and hTERT inhibition by MST-312 could further exacerbate this effect. Lowering the mitochondrial ROS level by MitoTEMPO could partially counteract the induction of cellular senescence induced by carbon-ion radiation and MST-312 incubation. Taken together, the current data suggest that telomere-mitochondrion links play a role in the induction of senescence in MCF-7 cells after carbon-ion irradiation.

#Telomere #mitochondrion #senescence #carbon-ion irradiation

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Miao, Guo-Ying

소속기관 Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences