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Yang H, Song Z, Wu X, Wu Y, Liu C. Onco Targets Ther. 2019;12:5563–5575. The Editor and Publisher of OncoTargets and Therapy wish to retract the published article. Concerns were raised over alleged image duplication in Figures 2D and 8B with similar images from unrelated articles, specifically: Figure 2D, panel T98 agomiR-652 appears to have been duplicated with a similar image in Figure 6C from Cheng et al, (https://doi.org/10.2147/OTT.S218876). Figure 8B appears to have been duplicated with similar images in Figure 7A from Ren et al, 2019 (http://www.ajcr.us/files/ajcr0088433.pdf). The authors did not respond to our queries and the Editor determined the findings of the study were no longer valid and advised for the article to be retracted. 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 The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”. This retraction relates to this paper

Song Z, Yang H, Wu X, Kong C, Xu C. Onco Targets Ther. 2019;12:4869–4881. The Editor and Publisher of OncoTargets and Therapy wish to retract the published article. Concerns were raised over alleged image duplication in Figures 2C and 8A with similar images from unrelated articles, specifically: Figure 2C, panel HTH83 miR-564 mimics appears to have been duplicated with a similar image in Figure 5D from Wang et al, 2018 (https://doi.org/10.3892/ijo.2019.4759). Figure 8A appears to have been duplicated with similar images in Figure 8A from Yun et al, 2019 (https://doi.org/10.2147/CMAR.S198615). The authors did not respond to our queries and the Editor determined the findings of the study were no longer valid and advised for the article to be retracted. 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 The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”. This retraction relates to this paper

This paper has been retracted.Huimei Yang, 1 Zhenzhen Song, 1 Xia Wu, 2 Yilei Wu, 2 Chengxia Liu 3 1Department of Laboratory, The Third People’s Hospital of Linyi, Linyi, Shandong 276023, People’s Republic of China; 2Department of Oncology, The Third People’s Hospital of Linyi, Linyi, Shandong 276023, People’s Republic of China; 3Department of Pathology, Linyi Cancer Hospital, Linyi, Shandong 276023, People’s Republic of ChinaPurpose: An increasing number of studies have documented that dysregulation of microRNAs (miRNAs) is common in glioblastoma multiforme (GBM). miR-652 is aberrantly expressed in various human cancers and plays important roles in numerous cancer-related processes. However, the expression profiles and potential roles of miR-652 in GBM remain largely unknown.Patients and methods: Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to determine miR-652 expression in GBM tissues and cell lines. The effects of miR-652 upregulation on GBM cell proliferation, clone formation, apoptosis, migration and invasion were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, clone formation, flow cytometry and Transwell® migration and invasion assays, respectively. In vivo xenotransplantation was utilized to determine the effect of miR-652 on GBM tumor growth in vivo. Of note, the molecular mechanisms underlying the tumor-suppressing activity of miR-652 upregulation in GBM cells were also investigated using a series of experiments, including bioinformatics analysis, luciferase reporter assay, RT-qPCR and Western blot analysis.Results: miR-652 expression was considerably downregulated in GBM tissues and cell lines. Low miR-652 expression was strongly correlated with Karnofsky performance score and tumor size. Overall survival duration was shorter in GBM patients with low miR-652 expression than in those with high miR-652 expression. miR-652

This paper has been retracted.Zhenzhen Song, 1 Huimei Yang, 1 Xia Wu, 2 Cui Kong, 2 Cong’e Xu 3 1Department of Laboratory, The Third People’s Hospital of Linyi, Linyi, Shandong 276023, People’s Republic of China; 2Department of Oncology, The Third People’s Hospital of Linyi, Linyi, Shandong 276023, People’s Republic of China; 3Department of Radiation Oncology, Linyi Cancer Hospital, Linyi, Shandong 276000, People’s Republic of ChinaBackground: Accumulating evidence has revealed that an increasing number of microRNAs (miRNAs) are dysregulated in papillary thyroid cancer (PTC) and that their dysregulation plays an important role in PTC onset and progression. Reportedly, miRNA-564 (miR-564) is downregulated in several types of human cancer. However, its expression profile and specific functions in PTC remain unclear to date.Methods: In this study, we used reverse transcription-quantitative polymerase chain reaction to detect miR-564 expression in PTC tissues and cell lines. Further, the regulatory roles of miR-564 in the malignant development of PTC in vitro and in vivo were examined using a series of functional experiments. In addition, the possible underlying mechanisms and signaling pathways involved were investigated.Results: We demonstrated that miR-564 expression markedly decreased in PTC tissues and cell lines, and this decrease correlated with the lymph node metastasis and tumor–node–metastasis stage. miR-564 upregulation significantly inhibited cell proliferation, migration, and invasion and induced cell apoptosis in vitro as well as hindered tumor growth in vivo. Furthermore, astrocyte-elevated gene-1 (AEG-1) was identified as a direct target gene of miR-564 in PTC cells. Its expression was upregulated and inversely correlated with miR-564 expression in clinically PTC tissues. Additionally, the silencing of AEG-1 expression could imitate the action of miR-564 overexpression in PTC