We aimed to explore the tolerance of esophageal cancer cells to radiation and to observe the morphological and gene expression changes in the cells following irradiation. The esophageal cancer cell line, Eca109, was cultured in vitro and was irradiated with a 6-MeV electron beam at a dose of 3 Gy once every other day, resulting in a cumulative dose of 15 Gy to 21 Gy. After radiotherapy, total RNA was extracted and was analyzed using a whole-transcription expression chip, and non-irradiated Eca109 cells were used as control. Gene ontology and pathway analyses were then performed on the differentially expressed genes. Approximately 99% of adherent cells were transformed into giant, malformed, multinucleated cells with mitotic catastrophe. One week after radiation was ceased, cells with normal morphology were observed adjacent to the cells with mitotic catastrophe, and over time, they formed clones. Ribosomal biosynthesis, mitotic nuclear division biological processes, and ubiquitin-mediated proteolysis might be the important mechanisms involved in radiation-induced mitotic catastrophe.

我们旨在探索食道癌细胞对放射线的耐受性，并观察放射线照射后细胞的形态和基因表达变化。食管癌细胞系Eca109在体外培养每隔一天以3 Gy的剂量照射6-MeV电子束，累积剂量为15 Gy至21 Gy。放疗后，提取总RNA并使用全转录表达芯片进行分析，并将未照射的Eca109细胞用作对照。然后对差异表达的基因进行基因本体论和途径分析。大约99％的贴壁细胞被转化为有丝分裂灾难的畸形巨核巨细胞。停止辐射一周后，观察到形态正常的细胞与有丝分裂灾难的细胞相邻，随着时间的推移，它们形成了克隆。核糖体的生物合成，核分裂的核生物过程，