TY - JOUR AB - 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. AD - 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 AU - Hong,Darong AU - Park,Min‑Ju AU - Jang,Eun ,Hyang AU - Jung,Bom AU - Kim,Nam‑Jung AU - Kim,Jong‑Ho DA - 2017/10/01 DO - 10.3892/ol.2017.6789 EP - 4872 IS - 4 JO - Oncol Lett KW - hispolon epithelial‑mesenchymal transition transforming growth factor β migration invasion PY - 2017 SN - 1792-1074 1792-1082 SP - 4866 ST - 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 T2 - Oncology Letters TI - 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 UR - https://doi.org/10.3892/ol.2017.6789 VL - 14 ER -