Autophagy promotes radiation-induced senescence but inhibits bystander effects in human breast cancer cells

Yao Huei Huang, Pei Ming Yang, Qiu Yu Chuah, Yi Jang Lee, Yi Fen Hsieh, Chih Wen Peng, Shu Jun Chiu

研究成果: 雜誌貢獻文章同行評審

36 引文 斯高帕斯(Scopus)

摘要

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.
原文英語
頁(從 - 到)1212-1228
頁數17
期刊Autophagy
10
發行號7
DOIs
出版狀態已發佈 - 2014

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Medicine(all)

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