Reactive oxygen species-driven mitochondrial injury induces apoptosis by teroxirone in human non-small cell lung cancer cells

Jing Ping Wang, Chang Heng Hsieh, Chun Yen Liu, Kai Han Lin, Pei Tsun Wu, Kwun Min Chen, Kang Fang

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11 Citations (Scopus)


Teroxirone as an anticancer agent is used to treat human lung cancer by inducing apoptotic cell death. Previous studies have demonstrated that the status of the tumor suppressor p53 determined the onset of apoptotic cell death in human non-small cell lung cancer cells (NSCLC). In order to further understand the underlying mechanisms of lung cancer, the present study explored the targets of teroxirone. By including antioxidants, the present study analyzed changes in cell proliferation, cell cycle division, mitochondrial membrane potential (MMP), reactive oxygen species (ROS), expression of apoptosis markers and cytochrome c distribution. Subsequent to a 12 h treatment with low concentrations of teroxirone, MMP was suppressed, followed by ROS production and apoptosis in lung cancer cells carrying wild type p53. N-acetylcysteine inhibited apoptotic cell death. The depleted expression of p53, reduction of apoptosis-associated active caspase-3 and poly ADP-ribose polymerase cleavage with resurgence of the pro-survival signal protein kinase B, all demonstrated an antioxidant-mediated reduction of apoptosis by teroxirone. The diminished ROS intensity inhibited the release of mitochondrial cytochrome c and DNA damage. The present study provided evidence that teroxirone treatment induced the ROS-activated intrinsic apoptotic pathway, which led to cell death in human NSCLC cells.

Original languageEnglish
Pages (from-to)3503-3509
Number of pages7
JournalOncology Letters
Issue number3
Publication statusPublished - 2017 Jan 1



  • Apoptosis
  • Mitochondria
  • Reactive oxygen species
  • Teroxirone

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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