Apoptosis and epithelial phagocytosis in mitomycin C-treated human pulmonary adenocarcinoma A549 cells.
Apoptosis and epithelial phagocytosis in mitomycin C-treated human pulmonary adenocarcinoma A549 cells.
复制标题
丝裂霉素 C 处理的人肺腺癌 A549 细胞的凋亡和上皮吞噬作用。
作者：
E. Simamura;Kei;H. Shimada;Junko Koyama
用电镜观察了丝裂霉素C损伤的人癌细胞的命运。在单层培养的肺腺癌A549细胞中，抗肿瘤药物丝裂霉素C诱导平滑肌内质网和高尔基体扩张。同时，在胞浆中形成髓鞘样结构、自噬体和致密的张力纤维束。核的变化还包括核仁浓缩，以及核小体的消失和边缘异染色质变薄。这些细胞核变得坚硬，染色质密集，最终导致细胞凋亡。线粒体和粗面内质网无明显改变。与此同时，一些剩余的完整的A549细胞将它们的细胞质向分离的细胞延伸并吞噬它们。这些结果表明，丝裂霉素C诱导A549细胞凋亡，同时刺激上皮细胞对自身受损细胞的吞噬活性。
Fate of human cancer cells damaged by mitomycin C was investigated by electron microscopy. In a monolayer culture of pulmonary adenocarcinoma A549 cells, the antitumor drug mitomycin C induced dilation of the smooth endoplasmic reticulum and Golgi apparatus. Simultaneously, the myelin figures, autophagosomes and dense tonofilament bundles were formed in the cytosol. Nuclear changes also included nucleolar condensation, as well as the disappearance of the karyosomes and thinned marginal heterochromatins. These nuclei came to be rigid and densely chromatic, finally resulting in apoptosis. There was no alteration in the mitochondria or rough endoplasmic reticulum. Meanwhile, some remaining intact A549 cells extended their cytoplasm toward detached cells and engulfed them. These results indicate that mitomycin C induces apoptosis in A549 cells and concurrently stimulates epithelial phagocytotic activity against their own damaged cells.