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Nelfinavir, an HIV protease inhibitor, induces apoptosis and cell cycle arrest in human cervical cancer cells via the ROS-dependent mitochondrial pathway  期刊论文  

  • 编号:
    99ed01d7-ff9d-4a3e-96c6-b83880dfa5a5
  • 作者:
    Xiang, Tong[1,2];Du, Lanying[1];Pham, Petra[1];Zhu, Bo[2];Jiang, Shibo(姜世勃)[1,3,4,5]
  • 语种:
    English
  • 期刊:
    CANCER LETTERS ISSN:0304-3835 2015 年 364 卷 1 期 (79 - 88) ; AUG 1
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  • 摘要:

    HIV protease inhibitors (HIV-PIs) are a class of antiretroviral drugs designed to target the viral protease. Strikingly, these drugs have also been reported to possess antitumor effect. In this study, we evaluated the activity of one HIV-PI, Nelfinavir, against human cervical cancer cells. We found that Nelfinavir inhibited the growth of cervical cancer cell lines at the lowest micromolar concentrations clinically attainable. Nelfinavir promoted apoptosis and arrested the cell cycle at Cl phase. Apoptosis is attributed to the promotion of mitochondrial reactive oxygen species (ROS) production, which results in the translocation of mitochondrial apoptosis inducing factor (AIF) to the nucleus. We further showed that Nelfinavir increased mitochondrial ROS production by decreasing manganese superoxide dismutase (MnSOD) protein levels. Taken together, our results suggest that Nelfinavir can be repositioned as a cervical cancer therapeutic. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

  • 推荐引用方式
    GB/T 7714:
    Xiang Tong,Du Lanying,Pham Petra, et al. Nelfinavir, an HIV protease inhibitor, induces apoptosis and cell cycle arrest in human cervical cancer cells via the ROS-dependent mitochondrial pathway [J].CANCER LETTERS,2015,364(1):79-88.
  • APA:
    Xiang Tong,Du Lanying,Pham Petra,Zhu Bo,&Jiang Shibo.(2015).Nelfinavir, an HIV protease inhibitor, induces apoptosis and cell cycle arrest in human cervical cancer cells via the ROS-dependent mitochondrial pathway .CANCER LETTERS,364(1):79-88.
  • MLA:
    Xiang Tong, et al. "Nelfinavir, an HIV protease inhibitor, induces apoptosis and cell cycle arrest in human cervical cancer cells via the ROS-dependent mitochondrial pathway" .CANCER LETTERS 364,1(2015):79-88.
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