Autophagy promotes radiation-induced senescence but inhibits bystander effects in human breast cancer cells
| العنوان: | Autophagy promotes radiation-induced senescence but inhibits bystander effects in human breast cancer cells |
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| المؤلفون: | Yi Jang Lee, Chih Wen Peng, Yao Huei Huang, Qiu Yu Chuah, Shu Jun Chiu, Yi Fen Hsieh, Pei Ming Yang |
| المصدر: | Autophagy. 10:1212-1228 |
| بيانات النشر: | Informa UK Limited, 2014. |
| سنة النشر: | 2014 |
| مصطلحات موضوعية: | STAT3 Transcription Factor, Senescence, Breast Neoplasms, Endogeny, Biology, Models, Biological, Cell Movement, Cell Line, Tumor, Phagosomes, Radiation, Ionizing, Autophagy, Bystander effect, Animals, Humans, Neoplasm Invasiveness, Molecular Biology, Protein kinase B, Cellular Senescence, Granulocyte-Macrophage Colony-Stimulating Factor, Bystander Effect, Cell Biology, Janus Kinase 2, Basic Research Paper, Cell biology, Securin, Tumor progression, Cancer cell, Cancer research, Female, Chickens, Proto-Oncogene Proteins c-akt, Cell aging, Signal Transduction |
| الوصف: | Ionizing radiation induces cellular senescence to suppress cancer cell proliferation. However, it also induces deleterious bystander effects in the unirradiated neighboring cells through the release of senescence-associated secretory phenotypes (SASPs) that promote tumor progression. Although autophagy has been reported to promote senescence, its role is still unclear. We previously showed that radiation induces senescence in PTTG1-depleted cancer cells. In this study, we found that autophagy was required for the radiation-induced senescence in PTTG1-depleted breast cancer cells. Inhibition of autophagy caused the cells to switch from radiation-induced senescence to apoptosis. Senescent cancer cells exerted bystander effects by promoting the invasion and migration of unirradiated cells through the release of CSF2 and the subsequently activation of the JAK2-STAT3 and AKT pathways. However, the radiation-induced bystander effects were correlated with the inhibition of endogenous autophagy in bystander cells, which also resulted from the activation of the CSF2-JAK2 pathway. The induction of autophagy by rapamycin reduced the radiation-induced bystander effects. This study reveals, for the first time, the dual role of autophagy in radiation-induced senescence and bystander effects. |
| تدمد: | 1554-8635 1554-8627 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::19e5c4e6138e28e3d88ca7ecf9196dbbTest https://doi.org/10.4161/auto.28772Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....19e5c4e6138e28e3d88ca7ecf9196dbb |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15548635 15548627 |
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