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Article

Paeoniflorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling

  • Authors:
    • Nanmu Yang
    • Hong Cui
    • Feng Han
    • Ling Zhang
    • Tao Huang
    • Yi Zhou
    • Jinxue Zhou
  • View Affiliations / Copyright

    Affiliations: Department of Hepatopancreatobiliary Surgery, The Affiliated Tumor Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou, Henan 450008, P.R. China
  • Pages: 1471-1476
    |
    Published online on: June 22, 2016
       https://doi.org/10.3892/ol.2016.4761
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Abstract

Paeoniflorin exhibits anticancer, anti-inflammatory and antioxidation effects, as well as specific pharmacological effects on smooth muscle and the immune, cardiovascular and central nervous systems. The present study aimed to investigate the anticancer effects of paeoniflorin on pancreatic cancer cells and to elucidate the mechanisms by which these effects occur. In the present study, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assays were performed to assess cell viability and cell cytotoxicity of BXPC‑3 human pancreatic cancer cells, respectively. Cellular apoptosis and caspase-3/9 activities were analyzed using an Annexin V‑fluorescein isothiocyanate/propidium iodide Apoptosis Detection kit, a DAPI staining assay and colorimetric kits, respectively. Matrix metalloproteinase‑9 (MMP‑9) and extracellular signal-regulated kinases (ERK) protein expression in BXPC‑3 cells were also investigated using gelatin zymography assays and western blot analysis, respectively. In the present study, paeoniflorin was found to inhibit the cell viability and increase cell cytotoxicity of BXPC‑3 cells in a dose‑ and time‑dependent manner. In addition, cellular apoptosis, as well as caspase‑3 and ‑9 activity of BXPC‑3 cells was increased following paeoniflorin treatment. Notably, paeoniflorin reduced MMP‑9 and ERK protein expression in BXPC‑3 cells. These results indicate that paeoniflorin exhibits a potential anticancer effect by enhancing human pancreatic cancer cell apoptosis via the suppression of MMP-9 and ERK signaling.
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Copy and paste a formatted citation
Spandidos Publications style
Yang N, Cui H, Han F, Zhang L, Huang T, Zhou Y and Zhou J: Paeoniflorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling. Oncol Lett 12: 1471-1476, 2016.
APA
Yang, N., Cui, H., Han, F., Zhang, L., Huang, T., Zhou, Y., & Zhou, J. (2016). Paeoniflorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling. Oncology Letters, 12, 1471-1476. https://doi.org/10.3892/ol.2016.4761
MLA
Yang, N., Cui, H., Han, F., Zhang, L., Huang, T., Zhou, Y., Zhou, J."Paeoniflorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling". Oncology Letters 12.2 (2016): 1471-1476.
Chicago
Yang, N., Cui, H., Han, F., Zhang, L., Huang, T., Zhou, Y., Zhou, J."Paeoniflorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling". Oncology Letters 12, no. 2 (2016): 1471-1476. https://doi.org/10.3892/ol.2016.4761
Copy and paste a formatted citation
x
Spandidos Publications style
Yang N, Cui H, Han F, Zhang L, Huang T, Zhou Y and Zhou J: Paeoniflorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling. Oncol Lett 12: 1471-1476, 2016.
APA
Yang, N., Cui, H., Han, F., Zhang, L., Huang, T., Zhou, Y., & Zhou, J. (2016). Paeoniflorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling. Oncology Letters, 12, 1471-1476. https://doi.org/10.3892/ol.2016.4761
MLA
Yang, N., Cui, H., Han, F., Zhang, L., Huang, T., Zhou, Y., Zhou, J."Paeoniflorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling". Oncology Letters 12.2 (2016): 1471-1476.
Chicago
Yang, N., Cui, H., Han, F., Zhang, L., Huang, T., Zhou, Y., Zhou, J."Paeoniflorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling". Oncology Letters 12, no. 2 (2016): 1471-1476. https://doi.org/10.3892/ol.2016.4761
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