Author of

• 18272

  +

  P3.01 - Poster Session with Presenters Present (ID 469)

  • Event: WCLC 2016
  • Type: Poster Presenters Present
  • Track: Biology/Pathology
  • Presentations: 1
  • Moderators:
  • Coordinates: 12/07/2016, 14:30 - 15:45, Hall B (Poster Area)

  • 18313

    +

    P3.01-041 - Anti-Cancer Effect of Hyperoxia on Human Lung Cancer Cells through Oxidative Stress Mediated ERK Signaling (ID 4720)

    14:30 - 14:30  |  Author(s): S.H. Lee
    • Abstract

    Background:
    Abnormal increases in reactive oxygen species (ROS) in cancer cells serves as a target for tumor-selective killing. Also, several experimental and clinical trials studied the effect of the hyperoxia condition by difference of response between normal cells and cancer cells. In this study, the hypothesis tested was that normobaric high oxygen concentration would have anti-cancer effects such as inducing apoptosis on human lung cancer cell line.
    
    Methods:
    Human bronchial epithelial cells (Beas-2b) and human alveolar adenocarcinoma cells (A549) were exposed with hyperoxia condition in a time-dependent manner. The changes in the cell morphology, viability and protein expressions such as p53 and ERK were examined after the exposure of hyperoxia (90% O~2~). In addition, to investigate whether hyperoxia condition affects the production of ROS and cell cycle regulation, cells were analyzed by a flow cytometry.
    
    Results:
    Exposure to the hyperoxia caused morphologic changes such as atypical nuclei and numerous mitotic figures which inhibited the cell viability in a time-dependent manner in A549 (p <0.01). In addition, the colony formation was suppressed selectively in A549 exposed to hyperoxia. Although not statistically significant, A549 exposed to hyperoxia showed increases in the ROS levels compared with Beas-2b. Also, the hyperoxia condition caused a progression delay in the G2/M cell cycle significantly in A549 (p <0.01). In hyperoxia exposed A549 cells, the phosphorylation of ERK 1/2 (p-ERK 1/2) was reduced while the phosphorylation of p53 was increased.
    
    Conclusion:
    This study showed that hyperoxia may have anti-cancer effect by decreasing cell viability and the colony forming ability. ROS generation by hyperoxia may cause to suppress the p-ERK, it related with the activation of p53 and G2/M cell cycle arrest. In conclusion, our data suggests that the anti-cancer effect of hyperoxia may relate to the ROS through oxidative stress mediated ERK signaling and cell arrest.