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Lu JJ, Xu Y, Zhao Z, et al. Onco Targets Ther. 2017;10:3579–3589. 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 The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”.

Xuan Zong,1 Jia-Xin Yang,1 Ying Zhang,1 Dong-Yan Cao,1 Keng Shen,1 Yan You,2 Li-Na Guo2 1Department of Obstetrics and Gynecology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People’s Republic of China; 2Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People’s Republic of China Abstract: 46, XY pure gonadal dysgenesis (PGD) is characterized as a female phenotype with strip-like gonads, which has a high tendency to develop into gonadal tumors. Somatic-type malignancies of germ cell tumors (SMs of GCTs) refer to the presence of malignant non-germ cell histologies admixed with GCTs, which are usually chemoresistant and indicate poor prognosis. This case report aimed to analyze the special histological type of GCTs and the importance of salvage surgery in the treatment of refractory GCTs. We report a unique case of gonadal yolk sac tumor (YST) transformed into SMs in a patient with 46, XY PGD. This 18-year-old woman underwent laparoscopic pelvic tumor resection, considered her first surgery, 2 years ago, and pathology revealed YST with initial alpha-fetoprotein (AFP) level measuring >3,000 ng/mL. She underwent seven cycles of chemotherapy, and the AFP level decreased to within a normal range after the second cycle. However, a computed tomography scan after the seventh cycle revealed abdominal and pelvic metastases, and vaginal bleeding was continuously observed. Laparoscopic exploration and laparotomy with tumor subtotal resection were performed. A pathology report showed SMs (sarcoma) derived from YST. Whole exome sequencing demonstrated that the main somatic mutation was a non-synonymous mutation of KRAS (c.182A>G), and this result did not show any indications for targeted drugs. She received three cycles of PEI (cisplatin, etoposide, and ifosfamide) chemotherapy but showed no response. She refused to undergo further treatment and has been alive with the disease for 7 months. This suggests that SMs may be one of the reasons for chemoresistance of refractory GCTs, and salvage surgery may be one of the most effective treatments for this patient. Targeted therapy may be a new choice for chemoresistant GCTs, but drug selection must be based on gene sequencing, and its efficacy still needs to be verified by further study. Keywords: disorder of sex development, germ cell tumor, somatic-type malignancy, salvage surgery

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