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Open AccessArticle

11-epi-Sinulariolide Acetate Reduces Cell Migration and Invasion of Human Hepatocellular Carcinoma by Reducing the Activation of ERK1/2, p38MAPK and FAK/PI3K/AKT/mTOR Signaling Pathways

1
Graduate Institute of Veterinary Medicine, National Pingtung University of Science and Technology, Pingtung 91202, Taiwan
2
National Museum of Marine Biology and Aquarium, Pingtung 94450, Taiwan
3
Kaohsiung District Agricultural Improvement Station, Pingtung 900, Taiwan
4
Department of Physical Medicine and Rehabilitation, Kaohsiung Medical University Hospital, Kaohsiung 80761, Taiwan
5
Department of Beauty Science, Meiho University, Pingtung 91202, Taiwan
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Mar. Drugs 2014, 12(9), 4783-4798; https://doi.org/10.3390/md12094783
Received: 27 May 2014 / Revised: 11 August 2014 / Accepted: 22 August 2014 / Published: 12 September 2014
Cancer metastasis is one of the major causes of death in cancer. An active compound, 11-epi-sinulariolide acetate (11-epi-SA), isolated from the cultured soft coral Sinularia flexibilis has been examined for potential anti-cell migration and invasion effects on hepatocellular carcinoma cells (HCC). However, the molecular mechanism of anti-migration and invasion by 11-epi-SA on HCC, along with their corresponding effects, remain poorly understood. In this study, we investigated anti-migration and invasion effects and the underlying mechanism of 11-epi-SA in HA22T cells, and discovered by trans-well migration and invasion assays that 11-epi-SA provided a concentration-dependent inhibitory effect on the migration of human HCC HA22T cells. After treatment with 11-epi-SA for 24 h, there were suppressed protein levels of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) and urokinase-type plasminogen activator (uPA) in HA22T cells. Meanwhile, the expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) and metalloproteinase-2 (TIMP-2) were increased in a concentration-dependent manner. Further investigation revealed that 11-epi-SA suppressed the phosphorylation of ERK1/2 and p38MAPK. The 11-epi-SA also suppressed the expression of the phosphorylation of FAK/PI3K/AKT/mTOR pathways. View Full-Text
Keywords: 11-epi-sinulariolide acetate; hepatocellular carcinoma; migration; invasion; matrix metalloproteinase; ERK1/2; p38MAPK 11-epi-sinulariolide acetate; hepatocellular carcinoma; migration; invasion; matrix metalloproteinase; ERK1/2; p38MAPK
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MDPI and ACS Style

Lin, J.-J.; Su, J.-H.; Tsai, C.-C.; Chen, Y.-J.; Liao, M.-H.; Wu, Y.-J. 11-epi-Sinulariolide Acetate Reduces Cell Migration and Invasion of Human Hepatocellular Carcinoma by Reducing the Activation of ERK1/2, p38MAPK and FAK/PI3K/AKT/mTOR Signaling Pathways. Mar. Drugs 2014, 12, 4783-4798.

AMA Style

Lin J-J, Su J-H, Tsai C-C, Chen Y-J, Liao M-H, Wu Y-J. 11-epi-Sinulariolide Acetate Reduces Cell Migration and Invasion of Human Hepatocellular Carcinoma by Reducing the Activation of ERK1/2, p38MAPK and FAK/PI3K/AKT/mTOR Signaling Pathways. Marine Drugs. 2014; 12(9):4783-4798.

Chicago/Turabian Style

Lin, Jen-Jie; Su, Jui-Hsin; Tsai, Chi-Chu; Chen, Yi-Jen; Liao, Ming-Hui; Wu, Yu-Jen. 2014. "11-epi-Sinulariolide Acetate Reduces Cell Migration and Invasion of Human Hepatocellular Carcinoma by Reducing the Activation of ERK1/2, p38MAPK and FAK/PI3K/AKT/mTOR Signaling Pathways" Mar. Drugs 12, no. 9: 4783-4798.

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