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Article

Honokiol inhibits bladder cancer cell invasion through repressing SRC‑3 expression and epithelial‑mesenchymal transition

  • Authors:
    • Lan Shen
    • Fang Zhang
    • Ruimin Huang
    • Jun Yan
    • Bing Shen
  • View Affiliations / Copyright

    Affiliations: State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing, Jiangsu 210061, P.R. China, Department of Urology, Shanghai General Hospital, Shanghai Jiaotong University, Shanghai 200080, P.R. China, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, P.R. China
  • Pages: 4294-4300
    |
    Published online on: July 25, 2017
       https://doi.org/10.3892/ol.2017.6665
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Abstract

Urinary bladder cancer (UBC) is one of the most common urological cancer types. Muscle invasive bladder cancer possesses high propensity for metastasis with poor prognosis. Honokiol is a lignan isolated from Magnolia officinalis with high bioavailability and potent anticancer effects. The results of the present study demonstrated that honokiol significantly inhibited UBC cell migration and invasion in a dose‑dependent manner compared with the vehicle‑treated control group. In addition, honokiol treatment suppressed epithelial‑mesenchymal transition by induction of E‑cadherin and repression of N‑cadherin. Honokiol was capable of significantly downregulating the expression of cell invasion‑associated genes, steroid receptor coactivator‑3 (SRC‑3), matrix metalloproteinase (MMP)‑2 and Twist1. Notably, the inhibition of UBC cell invasion by honokiol was reversed by reintroduction of oncoprotein SRC‑3 expression, with the restoration of MMP‑2 and Twist1, and reduction of E‑cadherin expression. Furthermore, the results of the luciferase assay confirmed that SRC‑3 could regulate Twist1 promoter activity. Taken together, the results of the present study suggest that honokiol is a promising agent against UBC cell invasion via downregulation of SRC‑3 and its target genes.
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Copy and paste a formatted citation
Spandidos Publications style
Shen L, Zhang F, Huang R, Yan J and Shen B: Honokiol inhibits bladder cancer cell invasion through repressing SRC‑3 expression and epithelial‑mesenchymal transition. Oncol Lett 14: 4294-4300, 2017.
APA
Shen, L., Zhang, F., Huang, R., Yan, J., & Shen, B. (2017). Honokiol inhibits bladder cancer cell invasion through repressing SRC‑3 expression and epithelial‑mesenchymal transition. Oncology Letters, 14, 4294-4300. https://doi.org/10.3892/ol.2017.6665
MLA
Shen, L., Zhang, F., Huang, R., Yan, J., Shen, B."Honokiol inhibits bladder cancer cell invasion through repressing SRC‑3 expression and epithelial‑mesenchymal transition". Oncology Letters 14.4 (2017): 4294-4300.
Chicago
Shen, L., Zhang, F., Huang, R., Yan, J., Shen, B."Honokiol inhibits bladder cancer cell invasion through repressing SRC‑3 expression and epithelial‑mesenchymal transition". Oncology Letters 14, no. 4 (2017): 4294-4300. https://doi.org/10.3892/ol.2017.6665
Copy and paste a formatted citation
x
Spandidos Publications style
Shen L, Zhang F, Huang R, Yan J and Shen B: Honokiol inhibits bladder cancer cell invasion through repressing SRC‑3 expression and epithelial‑mesenchymal transition. Oncol Lett 14: 4294-4300, 2017.
APA
Shen, L., Zhang, F., Huang, R., Yan, J., & Shen, B. (2017). Honokiol inhibits bladder cancer cell invasion through repressing SRC‑3 expression and epithelial‑mesenchymal transition. Oncology Letters, 14, 4294-4300. https://doi.org/10.3892/ol.2017.6665
MLA
Shen, L., Zhang, F., Huang, R., Yan, J., Shen, B."Honokiol inhibits bladder cancer cell invasion through repressing SRC‑3 expression and epithelial‑mesenchymal transition". Oncology Letters 14.4 (2017): 4294-4300.
Chicago
Shen, L., Zhang, F., Huang, R., Yan, J., Shen, B."Honokiol inhibits bladder cancer cell invasion through repressing SRC‑3 expression and epithelial‑mesenchymal transition". Oncology Letters 14, no. 4 (2017): 4294-4300. https://doi.org/10.3892/ol.2017.6665
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