Division of Radiation Oncology, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
Department of Neurosurgery, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
Oncol Rep. 2021 Apr;45(4). doi: 10.3892/or.2021.7964. Epub 2021 Mar 2.
The precise mechanism of intercellular communication between cancer cells following radiation exposure is unclear. Exosomes are membrane‑enclosed small vesicles comprising lipid bilayers and are mediators of intercellular communication that transport a variety of intracellular components, including microRNAs (miRNAs or miRs). The present study aimed to identify novel roles of exosomes released from irradiated cells to neighboring cancer cells. In order to confirm the presence of exosomes in the human pancreatic cancer cell line MIAPaCa‑2, ultracentrifugation was performed followed by transmission electron microscopy and nanoparticle tracking analysis (NanoSight) using the exosome‑specific surface markers CD9 and CD63. Subsequent endocytosis of exosomes was confirmed by fluorescent microscopy. Cell survival following irradiation and the addition of exosomes was evaluated by colony forming assay. Expression levels of miRNAs in exosomes were then quantified by microarray analysis, while protein expression levels of Cu/Zn‑ and Mn‑superoxide dismutase (SOD1 and 2, respectively) enzymes in MIAPaCa‑2 cells were evaluated by western blotting. Results showed that the uptake of irradiated exosomes was significantly higher than that of non‑irradiated exosomes. Notably, irradiated exosomes induced higher intracellular levels of reactive oxygen species (ROS) and a higher frequency of DNA damage in MIAPaCa‑2 cells, as determined by fluorescent microscopy and immunocytochemistry, respectively. Moreover, six up‑ and five downregulated miRNAs were identified in 5 and 8 Gy‑irradiated cells using miRNA microarray analyses. Further analysis using miRNA mimics and reverse transcription‑quantitative PCR identified miR‑6823‑5p as a potential candidate to inhibit SOD1, leading to increased intracellular ROS levels and DNA damage. To the best of our knowledge, the present study is the first to demonstrate that irradiated exosomes enhance the radiation effect via increasing intracellular ROS levels in cancer cells. This contributes to improved understanding of the bystander effect of neighboring cancer cells.
辐射暴露后癌细胞之间精确的细胞间通讯机制尚不清楚。外泌体是由脂质双层组成的膜封闭的小囊泡,是细胞间通讯的介质,可转运多种细胞内成分,包括 microRNAs(miRNAs 或 miRs)。本研究旨在确定辐射细胞释放的外泌体对邻近癌细胞的新作用。为了确认人胰腺癌细胞系 MIAPaCa-2 中外泌体的存在,进行了超速离心,然后使用外泌体特异性表面标志物 CD9 和 CD63 通过透射电子显微镜和纳米颗粒跟踪分析(NanoSight)进行分析。通过荧光显微镜确认外泌体的内吞作用。通过集落形成测定评估照射后和添加外泌体后的细胞存活。然后通过微阵列分析定量外泌体中的 miRNA 表达水平,同时通过 Western blot 评估 MIAPaCa-2 细胞中 Cu/Zn-和 Mn-超氧化物歧化酶(SOD1 和 2)的蛋白表达水平。结果表明,照射的外泌体的摄取明显高于非照射的外泌体。值得注意的是,通过荧光显微镜和免疫细胞化学分别测定,照射的外泌体可诱导 MIAPaCa-2 细胞中更高水平的活性氧(ROS)和更高频率的 DNA 损伤。此外,通过 miRNA 微阵列分析鉴定出在 5Gy 和 8Gy 照射的细胞中存在 6 个上调和 5 个下调的 miRNA。使用 miRNA 模拟物和逆转录-定量 PCR 的进一步分析鉴定出 miR-6823-5p 作为抑制 SOD1 的潜在候选物,导致细胞内 ROS 水平和 DNA 损伤增加。据我们所知,本研究首次证明照射的外泌体通过增加癌细胞中细胞内 ROS 水平来增强辐射效应。这有助于更好地理解邻近癌细胞的旁观者效应。