Emodin suppresses proliferation, migration and invasion in ovarian cancer cells by down regulating ILK in vitro and in vivo
Authors: Xiaoning Ke
Zhe Zhao
Jingjing Lu
Ying Xu
Xuan Wei
Xuan Zong
Jia Kang
Peishu Liu
Hongluan Mao
Journal: OncoTargets and Therapy (2017)
Discipline: CLINICAL MEDICINE
Keywords: ILK; Slug; emodin; epithelial ovarian cancer; epithelial–mesenchymal transition
Affiliations: Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Shandong., Department of Obstetrics and Gynecology, Handan Central Hospital, Handan, People's Republic of China.

Abstract:  Objective: Although our previous studies have confirmed that 1, 3, 8-trihydroxy-6-methylant hraquinone (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. 

Retracted: No

PubPeer comments:
 Figure 1 and 2. * Red boxes: A possible overlap in Figure 1E, top row, between two panels * Blue boxes: A possible overlap between panels in Figure 1E, bottom row, and Figure 2C, bottom row ![file] ![file] , 
 Retracted [10 August 2022] . --------------------- At the authors request, the Editor and Publisher of OncoTargets and Therapy wish to retract the published article. The authors raised concerns after discovering the duplication of cell migration and invasion images in Figures 1 and 2. Specifically, - Figure 1E, A2780, Migration, Normal appears to have been duplicated with Figure 1E, A2780, Migration pLVX-Con. - Figure 1E, SK-OV-3, Invasion, Normal appears to have been duplicated with Figure 2C, SK-OV-3, Invasion, pLVX-Con+, pLVX-ILK-, Emodin-. The authors provided original data and requested to retract the article. All the authors agreed that the retraction was necessary for reasons of scientific accuracy. The Editor agreed with this decision. Our decision-making was informed by our policy on publishing ethics and integrity and the COPE guidelines on retraction. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as u201cRetractedu201d. ,