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Article

Neokestose suppresses the growth of human melanoma A2058 cells via inhibition of the nuclear factor‑κB signaling pathway

  • Authors:
    • Jiann‑Shing Wu
    • Jan‑Yi Chang
    • C. Will Chen
    • Ming‑Tse Lin
    • Dey‑Chyi Sheu
    • Shun‑Mei Lee
  • View Affiliations / Copyright

    Affiliations: Department of Styling and Cosmetology, Hsin Shen Junior College of Medical Care and Management, Taoyuan 325, Taiwan, R.O.C., Department of Bioengineering, Tatung University, Taipei 104, Taiwan, R.O.C.
  • Pages: 295-300
    |
    Published online on: May 17, 2017
       https://doi.org/10.3892/mmr.2017.6594
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Abstract

Neokestose has superior prebiotic effects compared with the commercial fructooligosaccharides (FOS). In addition, the branched structure of neokestose, a type of neo‑FOS, confers improved chemical stability compared with conventional FOS; therefore, the investigation of the branched structure by the present study may be of high biomedical value. The present study aimed to determine whether neokestose may suppress growth of the A2058 melanoma cell line. The cells were initially treated with neokestose; subsequently, in vitro cytotoxicity was assessed using MTT, and cell cycle progression and apoptosis were detected using flow cytometry. The protein expression levels of cyclin D1, phosphorylated (p)‑inhibitor of κB (IκB) and nuclear factor‑κB (NF‑κB) were determined using western blotting. Treatment with neokestose led to a dose‑dependent inhibition of cell viability. Flow cytometry data indicated that neokestose increased the sub‑G1 cell population, and induced early and late apoptosis. Western blot analysis revealed that neokestose treatment reduced the expression levels of p‑IκB and cyclin D1. These findings suggest that neokestose treatment may induce suppression of A2058 melanoma cell viability via inhibition of the NF‑κB pathway. The present findings support the requirement for further investigation into the potential use of neokestose as an additional or chemopreventive therapeutic agent for the treatment of melanoma.
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Copy and paste a formatted citation
Spandidos Publications style
Wu JS, Chang JY, Chen C, Lin MT, Sheu DC and Lee SM: Neokestose suppresses the growth of human melanoma A2058 cells via inhibition of the nuclear factor‑κB signaling pathway. Mol Med Rep 16: 295-300, 2017.
APA
Wu, J., Chang, J., Chen, C., Lin, M., Sheu, D., & Lee, S. (2017). Neokestose suppresses the growth of human melanoma A2058 cells via inhibition of the nuclear factor‑κB signaling pathway. Molecular Medicine Reports, 16, 295-300. https://doi.org/10.3892/mmr.2017.6594
MLA
Wu, J., Chang, J., Chen, C., Lin, M., Sheu, D., Lee, S."Neokestose suppresses the growth of human melanoma A2058 cells via inhibition of the nuclear factor‑κB signaling pathway". Molecular Medicine Reports 16.1 (2017): 295-300.
Chicago
Wu, J., Chang, J., Chen, C., Lin, M., Sheu, D., Lee, S."Neokestose suppresses the growth of human melanoma A2058 cells via inhibition of the nuclear factor‑κB signaling pathway". Molecular Medicine Reports 16, no. 1 (2017): 295-300. https://doi.org/10.3892/mmr.2017.6594
Copy and paste a formatted citation
x
Spandidos Publications style
Wu JS, Chang JY, Chen C, Lin MT, Sheu DC and Lee SM: Neokestose suppresses the growth of human melanoma A2058 cells via inhibition of the nuclear factor‑κB signaling pathway. Mol Med Rep 16: 295-300, 2017.
APA
Wu, J., Chang, J., Chen, C., Lin, M., Sheu, D., & Lee, S. (2017). Neokestose suppresses the growth of human melanoma A2058 cells via inhibition of the nuclear factor‑κB signaling pathway. Molecular Medicine Reports, 16, 295-300. https://doi.org/10.3892/mmr.2017.6594
MLA
Wu, J., Chang, J., Chen, C., Lin, M., Sheu, D., Lee, S."Neokestose suppresses the growth of human melanoma A2058 cells via inhibition of the nuclear factor‑κB signaling pathway". Molecular Medicine Reports 16.1 (2017): 295-300.
Chicago
Wu, J., Chang, J., Chen, C., Lin, M., Sheu, D., Lee, S."Neokestose suppresses the growth of human melanoma A2058 cells via inhibition of the nuclear factor‑κB signaling pathway". Molecular Medicine Reports 16, no. 1 (2017): 295-300. https://doi.org/10.3892/mmr.2017.6594
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