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Emodin suppresses proliferation, migration and invasion in ovarian cancer cells by down regulating ILK in vitro and in vivo

Authors Lu JJ, Xu Y, Zhao Z, Ke XN, Wei X, Kang J, Zong X, Mao HL, Liu PS

Received 29 March 2017

Accepted for publication 24 May 2017

Published 19 July 2017 Volume 2017:10 Pages 3579—3589


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Ashok Kumar Pandurangan

Peer reviewer comments 2

Editor who approved publication: Dr Ingrid Espinoza

Jingjing Lu,1,2,* Ying Xu,1,* Zhe Zhao,1 Xiaoning Ke,2 Xuan Wei,1 Jia Kang,1 Xuan Zong,1 Hongluan Mao,1 Peishu Liu1

1Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong, 2Department of Obstetrics and Gynecology, Handan Central Hospital, Handan, People’s Republic of China

*These authors contributed equally to this work

Objective: Although our previous studies have confirmed that 1, 3, 8-trihydroxy-6-methylanthraquinone (emodin) inhibits migration and invasion in epithelial ovarian cancer (EOC) cells, the underlying molecular mechanism remains unknown. Here, the aim was to investigate the effects of emodin on EOC cells and to study further the mechanism underlying this process, both in vitro and in vivo.
Materials and methods: Cell proliferation was evaluated by the methylthiazolyl tetrazolium assay. Cell migration and invasion abilities were tested using the transwell assay. The expression of integrin-linked kinase (ILK) and epithelial–mesenchymal transition (EMT)-associated factors were measured with western blotting.
Results: Exogenous ILK enhanced the proliferation, migration and invasion properties of A2780 and SK-OV-3 cells. After treatment with emodin, the survival rate of cells was gradually reduced, including those of SK-OV-3/pLVX-ILK and A2780/pLVX-ILK cells, with increasing emodin concentrations. The migration and invasion abilities of A2780 and SK-OV-3 cells were effectively increased by the transfection of pLVX-ILK, which could be abrogated by following this with 48 hours of emodin treatment. Treatment with emodin significantly downregulated the expression of ILK and EMT-related proteins. So, emodin suppressed proliferation, migration and invasion in ovarian cancer cells by downregulating ILK in vitro. SK-OV-3/pLVX-Con and SK-OV-3/pLVX-ILK cells were used to generate xenografts in nude mice. Tumors grew more rapidly in the SK-OV-3/pLVX-ILK group compared with the control group, and this could be significantly inhibited by emodin. Also, the expression of E-cadherin was downregulated, while the expression of Slug, MMP-9 and Vimentin were upregulated in the SK-OV-3/pLVX-ILK group, and this could be reversed by following treatment with emodin. Emodin did not demonstrate target toxicity on hepatocytes, nephrocytes and cardiomyocytes.
Conclusion: Emodin suppresses proliferation, migration and invasion in ovarian cancer by targeting ILK.

Keywords: emodin, ILK, epithelial ovarian cancer, epithelial–mesenchymal transition, Slug, xenografts in nude mice

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