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Article

Hispolon as an inhibitor of TGF‑β‑induced epithelial‑mesenchymal transition in human epithelial cancer cells by co‑regulation of TGF‑β‑Snail/Twist axis

  • Authors:
    • Darong Hong
    • Min‑Ju Park
    • Eun Hyang Jang
    • Bom Jung
    • Nam‑Jung Kim
    • Jong‑Ho Kim
  • View Affiliations / Copyright

    Affiliations: Department of Life and Nanopharmaceutical Science, Graduate School, Kyung Hee University, Dongdaemun‑gu, Seoul 02447, Republic of Korea, Department of Pharmacy, Graduate School, Kyung Hee University, Dongdaemun‑gu, Seoul 02447, Republic of Korea
  • Pages: 4866-4872
    |
    Published online on: August 23, 2017
       https://doi.org/10.3892/ol.2017.6789
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Abstract

Hispolon (HPL), isolated from Phellinus linteus, has been used to treat various types of pathology, including inflammation, gastroenteric disorders, lymphatic diseases and numerous cancer subtypes. HPL has previously been reported to demonstrate a significant therapeutic efficacy against various types of cancer cells, including melanoma, leukemia, hepatocarcinoma, bladder and gastric cancer cells. However, its potential role in the epithelial‑mesenchymal transition (EMT) has not been demonstrated. The present study investigated the effects of HPL on the EMT. Transforming growth factor β (TGF‑β) induced enhanced cell migration and invasion, EMT‑associated phenotypic changes. In the present study, HPL recovered the reduction of E‑cadherin expression level in TGF‑β treated cancer cells, which was regulated by the expression of Snail and Twist. HPL downregulated Snail and Twist, an effect that was enhanced by TGF‑β. These findings provide novel evidence that HPL suppresses cancer cell migration and invasion by inhibiting EMT. Therefore, HPL may be a potent anticancer agent, inhibiting metastasis.
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Copy and paste a formatted citation
Spandidos Publications style
Hong D, Park MJ, Jang EH, Jung B, Kim NJ and Kim JH: Hispolon as an inhibitor of TGF‑β‑induced epithelial‑mesenchymal transition in human epithelial cancer cells by co‑regulation of TGF‑β‑Snail/Twist axis. Oncol Lett 14: 4866-4872, 2017.
APA
Hong, D., Park, M., Jang, E.H., Jung, B., Kim, N., & Kim, J. (2017). Hispolon as an inhibitor of TGF‑β‑induced epithelial‑mesenchymal transition in human epithelial cancer cells by co‑regulation of TGF‑β‑Snail/Twist axis. Oncology Letters, 14, 4866-4872. https://doi.org/10.3892/ol.2017.6789
MLA
Hong, D., Park, M., Jang, E. H., Jung, B., Kim, N., Kim, J."Hispolon as an inhibitor of TGF‑β‑induced epithelial‑mesenchymal transition in human epithelial cancer cells by co‑regulation of TGF‑β‑Snail/Twist axis". Oncology Letters 14.4 (2017): 4866-4872.
Chicago
Hong, D., Park, M., Jang, E. H., Jung, B., Kim, N., Kim, J."Hispolon as an inhibitor of TGF‑β‑induced epithelial‑mesenchymal transition in human epithelial cancer cells by co‑regulation of TGF‑β‑Snail/Twist axis". Oncology Letters 14, no. 4 (2017): 4866-4872. https://doi.org/10.3892/ol.2017.6789
Copy and paste a formatted citation
x
Spandidos Publications style
Hong D, Park MJ, Jang EH, Jung B, Kim NJ and Kim JH: Hispolon as an inhibitor of TGF‑β‑induced epithelial‑mesenchymal transition in human epithelial cancer cells by co‑regulation of TGF‑β‑Snail/Twist axis. Oncol Lett 14: 4866-4872, 2017.
APA
Hong, D., Park, M., Jang, E.H., Jung, B., Kim, N., & Kim, J. (2017). Hispolon as an inhibitor of TGF‑β‑induced epithelial‑mesenchymal transition in human epithelial cancer cells by co‑regulation of TGF‑β‑Snail/Twist axis. Oncology Letters, 14, 4866-4872. https://doi.org/10.3892/ol.2017.6789
MLA
Hong, D., Park, M., Jang, E. H., Jung, B., Kim, N., Kim, J."Hispolon as an inhibitor of TGF‑β‑induced epithelial‑mesenchymal transition in human epithelial cancer cells by co‑regulation of TGF‑β‑Snail/Twist axis". Oncology Letters 14.4 (2017): 4866-4872.
Chicago
Hong, D., Park, M., Jang, E. H., Jung, B., Kim, N., Kim, J."Hispolon as an inhibitor of TGF‑β‑induced epithelial‑mesenchymal transition in human epithelial cancer cells by co‑regulation of TGF‑β‑Snail/Twist axis". Oncology Letters 14, no. 4 (2017): 4866-4872. https://doi.org/10.3892/ol.2017.6789
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