Emodin potentiates the antitumor effects of gemcitabine in pancreatic cancer cells via inhibition of nuclear factor-κB

  • Authors:
    • An Liu
    • Hui Chen
    • Hongfei Tong
    • Sheng Ye
    • Maixuan Qiu
    • Zhaohong Wang
    • Wei Tan
    • Jinxiang Liu
    • Shengzhang Lin
  • View Affiliations

  • Published online on: January 3, 2011     https://doi.org/10.3892/mmr.2011.414
  • Pages: 221-227
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Abstract

Many studies have demonstrated that emodin inhibits the growth and induces the apoptosis and chemo-sensitization of various cancer cells in animal models. The aim of this study was to investigate the molecular mechanism of the chemo-sensitization potential of emodin on gemcitabine in pancreatic cancer cell lines via inhibition of nuclear factor-κB (NF-κB). SW1990 and SW1990/GZ cells were treated with: i) emodin (20 µmol/l), ii) NF-κB inhibitor Bay 11-7082 (5 µmol/l), iii) gemcitabine (20 µmol/l), iv) pre-treated with emodin for 24 h followed by coincubation with gemcitabine for 24 h, or v) pre-treated with Bay 11-7082 for 1 h followed by treatment with gemcitabine for 24 h. SW1990 and SW1990/GZ cells were also treated with emodin (20, 40 and 80 µmol/l). Cellular proliferation and apoptosis were detected by the Cell Counting Kit-8 (CCK-8) assay and flow cytometry. NF-κB protein was detected by Western blotting. SW1990/GZ cell morphological changes were observed under optical and fluorescence microscopes. Emodin strongly inhibited the proliferation and induced the apoptosis of both pancreatic cancer cell lines. Furthermore, emodin combined with gemcitabine induced a higher percentage of growth inhibition and apoptosis in both pancreatic cancer cell lines compared to gemcitabine alone. Pre-treatment of SW1990/GZ cells with Bay 11-7082 for 1 h followed by gemcitabine resulted in greater inhibitory and apoptosis rates compared to gemcitabine alone. The resistant pancreatic cell line SW1990/GZ presented higher constitutive NF-κB protein expression compared to the SW1990 cells. Emodin not only down-regulated NF-κB in a dose-dependent manner in SW1990 and SW1990/GZ cells under unstimulated conditions, but also inhibited gemcitabine-induced NF-κB protein expression. Emodin potentiated the antitumor effects of gemcitabine in pancreatic cancer, which was related to the down-regulation of NF-κB.

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March-April 2011
Volume 4 Issue 2

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Liu A, Chen H, Tong H, Ye S, Qiu M, Wang Z, Tan W, Liu J and Lin S: Emodin potentiates the antitumor effects of gemcitabine in pancreatic cancer cells via inhibition of nuclear factor-κB. Mol Med Rep 4: 221-227, 2011
APA
Liu, A., Chen, H., Tong, H., Ye, S., Qiu, M., Wang, Z. ... Lin, S. (2011). Emodin potentiates the antitumor effects of gemcitabine in pancreatic cancer cells via inhibition of nuclear factor-κB. Molecular Medicine Reports, 4, 221-227. https://doi.org/10.3892/mmr.2011.414
MLA
Liu, A., Chen, H., Tong, H., Ye, S., Qiu, M., Wang, Z., Tan, W., Liu, J., Lin, S."Emodin potentiates the antitumor effects of gemcitabine in pancreatic cancer cells via inhibition of nuclear factor-κB". Molecular Medicine Reports 4.2 (2011): 221-227.
Chicago
Liu, A., Chen, H., Tong, H., Ye, S., Qiu, M., Wang, Z., Tan, W., Liu, J., Lin, S."Emodin potentiates the antitumor effects of gemcitabine in pancreatic cancer cells via inhibition of nuclear factor-κB". Molecular Medicine Reports 4, no. 2 (2011): 221-227. https://doi.org/10.3892/mmr.2011.414