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Article

Diallyl trisulfide induces osteosarcoma cell apoptosis through reactive oxygen species-mediated downregulation of the PI3K/Akt pathway

  • Authors:
    • Hongliang Wang
    • Na Sun
    • Xin Li
    • Ka Li
    • Jiguang Tian
    • Jianmin Li
  • View Affiliations / Copyright

    Affiliations: Department of Orthopedics, Qilu Hospital, Shandong University, Ji'nan, Shandong 250012, P.R. China, Shandong Institute of Medicine and Health Information, Shandong Academy of Medical Sciences, Ji'nan, Shandong 250062, P.R. China, Department of Emergency, Qilu Hospital, Shandong University, Ji'nan, Shandong 250012, P.R. China
  • Pages: 3648-3658
    |
    Published online on: April 1, 2016
       https://doi.org/10.3892/or.2016.4722
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Abstract

Diallyl trisulfide (DATS) is a natural organosulfur compound isolated from garlic, and has been reported to possess anticancer activities. However, the cancer growth inhibitory effects and molecular mechanisms in human osteosarcoma cells have not been well studied. The present study demonstrated that DATS significantly reduced cell viability in a dose- and time-dependent manner in MG63 and MNNG/HOS cells. DATS-induced G0/G1 phase arrest was found to correlate with a decrease in cyclin D1 in concomitance with an increase in p21 and p27. DATS induced a marked increase in reactive oxygen species (ROS) levels and collapse of mitochondrial membrane potential (Δψm) in the osteosarcoma cells. DATS induced apoptosis in the MG63 and MNNG/HOS cells via inhibition of the PI3K/Akt signaling pathway and through the mitochondrial apoptotic pathway. The efficiency of DATS basically approached the efficacy of LY294002, a specific PI3K inhibitor. However, N-acetylcysteine (NAC), a general ROS scavenger, completely blocked the DATS-induced ROS increase, inhibition of the PI3K/Akt pathway and cell apoptosis. Overall, DATS has the potential to be developed as a new anticancer drug. The mechanisms of action involve the ROS-mediated downregulation of the PI3K/Akt pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Wang H, Sun N, Li X, Li K, Tian J and Li J: Diallyl trisulfide induces osteosarcoma cell apoptosis through reactive oxygen species-mediated downregulation of the PI3K/Akt pathway. Oncol Rep 35: 3648-3658, 2016.
APA
Wang, H., Sun, N., Li, X., Li, K., Tian, J., & Li, J. (2016). Diallyl trisulfide induces osteosarcoma cell apoptosis through reactive oxygen species-mediated downregulation of the PI3K/Akt pathway. Oncology Reports, 35, 3648-3658. https://doi.org/10.3892/or.2016.4722
MLA
Wang, H., Sun, N., Li, X., Li, K., Tian, J., Li, J."Diallyl trisulfide induces osteosarcoma cell apoptosis through reactive oxygen species-mediated downregulation of the PI3K/Akt pathway". Oncology Reports 35.6 (2016): 3648-3658.
Chicago
Wang, H., Sun, N., Li, X., Li, K., Tian, J., Li, J."Diallyl trisulfide induces osteosarcoma cell apoptosis through reactive oxygen species-mediated downregulation of the PI3K/Akt pathway". Oncology Reports 35, no. 6 (2016): 3648-3658. https://doi.org/10.3892/or.2016.4722
Copy and paste a formatted citation
x
Spandidos Publications style
Wang H, Sun N, Li X, Li K, Tian J and Li J: Diallyl trisulfide induces osteosarcoma cell apoptosis through reactive oxygen species-mediated downregulation of the PI3K/Akt pathway. Oncol Rep 35: 3648-3658, 2016.
APA
Wang, H., Sun, N., Li, X., Li, K., Tian, J., & Li, J. (2016). Diallyl trisulfide induces osteosarcoma cell apoptosis through reactive oxygen species-mediated downregulation of the PI3K/Akt pathway. Oncology Reports, 35, 3648-3658. https://doi.org/10.3892/or.2016.4722
MLA
Wang, H., Sun, N., Li, X., Li, K., Tian, J., Li, J."Diallyl trisulfide induces osteosarcoma cell apoptosis through reactive oxygen species-mediated downregulation of the PI3K/Akt pathway". Oncology Reports 35.6 (2016): 3648-3658.
Chicago
Wang, H., Sun, N., Li, X., Li, K., Tian, J., Li, J."Diallyl trisulfide induces osteosarcoma cell apoptosis through reactive oxygen species-mediated downregulation of the PI3K/Akt pathway". Oncology Reports 35, no. 6 (2016): 3648-3658. https://doi.org/10.3892/or.2016.4722
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