AI Article Synopsis

  • The study investigates how boningmycin induces cellular senescence in human tumor cells, specifically comparing its effects on oral epithelial carcinoma KB cells and non-small cell lung cancer A549 cells.
  • Researchers used various methods, including cell growth assays and flow cytometry, to analyze the growth-inhibitory effects and the molecular changes, particularly focusing on the increase of reactive oxygen species (ROS) and the cell cycle arrest at the G2/M phase.
  • The findings suggest that boningmycin promotes cellular senescence, marked by increased levels of the protein P21, contributing to its potential as a tumor-suppressive agent, while higher doses lead to apoptosis.

Article Abstract

Cellular senescence is one of the important steps against tumor. This study was to observe the characteristics of boningmycin induced senescence of human tumor cells. MIT method and clone formation assay were used to detect the growth-inhibitory effect. Cellular senescence was detected with senescence-associated beta-galactosidase staining. Cell cycle distribution and accumulation of intracellular reactive oxygen species (ROS) were analyzed with flow cytometry. Protein expression was detected by Western blotting. The results showed that the growth-inhibitory effect of boningmycin was obviously stronger on human oral epithelial carcinoma KB cells than that on non-small cell lung cancer A549 cells. Comparison to the similar action of doxorubicin, that boningmycin induced the features of cellular senescence in both cell lines, its due to the arrest at G2/M phase and an increase of ROS level. The molecular senescence marker P21 increased significantly after boningmycin treatment at a dosage of 0.1 micromol x L(-1), whereas a higher concentration of it induced apoptosis. The results indicated that cellular senescence induced by boningmycin was one of its mechanisms in tumor suppression.

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