Abstract
Cytoplasm is an important target for the radiation-induced bystander effect (RIBE). In the present work, the critical role of protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway in the generation of RIBE signaling after X-ray irradiation and the rapid phosphorylation of Akt and mTOR was observed in the cytoplasm of irradiated human lung adenocarcinoma epithelial (A549) cells. Targeting A549 cytoplasts with individual protons from a microbeam showed that RIBE signal(s) mediated by the Akt/mTOR pathway were generated even in the absence of a cell nucleus. These results provide a new insight into the mechanisms driving the cytoplasmic response to irradiation and their impact on the production of RIBE signal(s).
Highlights
The radiation-induced bystander effect (RIBE), an example of a non-targeted effect of ionizing radiation, occurs when signal(s) released by the irradiated cells to activate neighboring or distal non-irradiated cells and cause effects similar to direct irradiation, including the induction of chromosomal aberrations, changes of specific gene expression, genomic instability, mutation or even neoplastic transformation [1]
We found that the protein kinase B (Akt)/mammalian target of rapamycin pathway activated in the X-irradiated cytoplasm played an important role in the production of RIBE signal(s)
We investigated the activation and role of RIBE-related cytoplasmic signaling, and we observed that the irradiation-activated proteinkinase B (Akt)/MK-2206 (Akt) or rapamycin (mTOR) pathway played an important role in the production of RIBE
Summary
The radiation-induced bystander effect (RIBE), an example of a non-targeted effect of ionizing radiation, occurs when signal(s) released by the irradiated cells to activate neighboring or distal non-irradiated cells and cause effects similar to direct irradiation, including the induction of chromosomal aberrations, changes of specific gene expression, genomic instability, mutation or even neoplastic transformation [1]. It is considered that RIBE can amplify the biological target area of radiation and cause genetic risks to the normal cells or tissues beyond the irradiated target in radiotherapy and other radiation exposures [1, 2]. It is speculated that the cytoplasm targeting causes mitochondrial activation and reactive oxygen species (ROS) production, the signal(s) transduce into nucleus to induce the irradiated cells to secret RIBE signal(s) [7,8,9]. It is pertinent to carry out experiments with more unambiguous designs to study the RIBE induced by cytoplasm irradiation in order to better understand the mechanisms underlying the production and transduction of relevant RIBE signal(s)
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