TY - JOUR ID - 32343 TI - Telomere-Mitochondrion Links Contribute to Induction of Senescence in MCF-7 Cells after Carbon-Ion Irradiation JO - Asian Pacific Journal of Cancer Prevention JA - APJCP LA - en SN - 1513-7368 AU - Miao, Guo-Ying AU - Zhou, Xin AU - Zhang, Xin AU - Xie, Yi AU - Sun, Chao AU - Liu, Yang AU - Gan, Lu AU - Zhang, Hong AD - Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences, Gansu Province, China AD - Y1 - 2016 PY - 2016 VL - 17 IS - 4 SP - 1993 EP - 1998 DO - N2 - 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 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. UR - https://journal.waocp.org/article_32343.html L1 - https://journal.waocp.org/article_32343_2678c55ab565619d89c03030785b3f6d.pdf ER -