Journal
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
Volume 2016, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2016/9460462
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Funding
- National Natural Science Foundation for Young Scholars [81402519]
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For many unresectable carcinomas and locally recurrent cancers (LRC), I-125 seeds brachytherapy is a feasible, effective, and safe treatment. Several studies have shown that I-125 seeds radiation exerts anticancer activity by triggering DNA damage. However, recent evidence shows mitochondrial quality to be another crucial determinant of cell fate, with mitophagy playing a central role in this control mechanism. Herein, we found that I-125 seeds irradiation injured mitochondria, leading to significantly elevated mitochondrial and intracellular ROS (reactive oxygen species) levels in HCT116 cells. The accumulation of mitochondrial ROS increased the expression of HIF-1 alpha and its target genes BINP3 and NIX (BINP3L), which subsequently triggered mitophagy. Importantly, I-125 seeds radiation induced mitophagy promoted cells survival and protected HCT116 cells from apoptosis. These results collectively indicated that I-125 seeds radiation triggered mitophagy by upregulating the level of ROS to promote cellular homeostasis and survival. The present study uncovered the critical role of mitophagy in modulating the sensitivity of tumor cells to radiation therapy and suggested that chemotherapy targeting on mitophagy might improve the efficiency of I-125 seeds radiation treatment, which might be of clinical significance in tumor therapy.
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