Apoptosis and epithelial phagocytosis in mitomycin C-treated human pulmonary adenocarcinoma A549 cells

Tissue Cell. 2001 Apr;33(2):161-8. doi: 10.1054/tice.2000.0167.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma*
  • Antibiotics, Antineoplastic / pharmacology
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Cell Nucleus / ultrastructure
  • Cytosol / ultrastructure
  • Endoplasmic Reticulum, Smooth / ultrastructure
  • Epithelial Cells / cytology*
  • Humans
  • Lung Neoplasms*
  • Microscopy, Electron
  • Mitomycin / pharmacology
  • Phagocytosis / physiology*
  • Tumor Cells, Cultured / cytology

Substances

  • Antibiotics, Antineoplastic
  • Mitomycin