The authors of the above article drew to our attention that they had identified three instances of data overlapping between data panels, suggesting that data purportedly showing results obtained under different experimental conditions had been derived from the same original source. Comparing between the two figures, two pairs of panels in Fig. 4B (the Mimics control and blank experiments for the U87 and U251 cell lines) were shown to be overlapping, and a further pair of panels showed overlapping data in Fig. 6B (the data panels for the miR‑375 mi + .pCDNA/RWDD3 and miR‑375 mi + .pCDNA experiments for the U87 cell line). The authors were able to re‑examine the original data files and retrieve the correct data panels. The errors in these figures arose through inadvertently assembling Figs. 4 and 6 incorrectly. The revised versions of Figs. 4 and 6, featuring the corrected data panels for the Mimics control and blank experiments for the U87 and U251 cell lines in Fig. 4B, and the correct data for the U87 cell line in Fig. 6B, are shown opposite and on the next page, respectively. Note that the corrections to the data shown in these Figures do not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in Oncology Reports 39: 1825-1834, 2018; DOI: 10.3892/or.2018.6261].
We previously reported that intraspinal transplantation of human amniotic mesenchymal stem cells (hAMSCs) promotes functional recovery in a rat model of acute traumatic spinal cord injury (SCI). However, whether intravenous transplantation of hAMSCs also has therapeutic benefit remains uncertain. In this study, we assessed whether intravenous transplantation of hAMSCs improves outcomes in rats with acute traumatic SCI. In addition, the potential mechanisms underlying the possible benefits of this therapy were investigated. Adult female Sprague–Dawley rats were subjected to SCI using a weight drop device, and then hAMSCs or PBS were administered after 2 h via the tail vein. Our results indicated that transplanted hAMSCs could migrate to injured spinal cord lesion. Compared with the control group, hAMSCs transplantation significantly decreased the numbers of ED1 + macrophages/microglia and caspase-3 + cells, and reduced levels of inflammatory cytokines, such as tumor necrosis factor alpha, interleukin-6 and IL-1β. In addition, hAMSCs transplantation significantly attenuated Evans blue extravasation, promoted angiogenesis and axonal regeneration. hAMSCs transplantation also significantly improved functional recovery. These results suggest that intravenous administration of hAMSCs provides neuroprotective effects in rats after acute SCI, and could be an alternative therapeutic approach for the treatment of acute SCI.
The authors of the above article drew to our attention that, in the above paper, they had identified three instances of data overlapping between data panels, suggesting that data purportedly showing results obtained under different experimental conditions had been derived from the same original source. Comparing among the data panels, two pairs of panels in Fig. 4B were shown to be overlapping, and a further pair of panels showed overlapping data in Fig. 6B. The authors were presented with an opportunity to correct their figures in a Corrigendum, although it has subsequently come to light that the replacement figures themselves featured problems with overlapping data. Given the errors that have been identified in the compilation of the figures in this article, the Editor of Oncology Reports has decided that this article should be retracted from the publication owing to a lack of overall confidence in the presented data. The authors all agree to the retraction of this article, and the Editor and the authors apologize for any inconvenience that might result from this retraction. [the original article was published in Oncology Reports 39: 1825-1834, 2018; DOI: 10.3892/or.2018.6261].
// Yang-Hua Fan 1, * , Min-Hua Ye 1, * , Lei Wu 1 , Miao-Jing Wu 1 , Shi-Gang Lu 1 , Xin-Gen Zhu 1 1 Department of Neurosurgery, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, People's Republic of China * These authors contributed equally to this work Correspondence to: Xin-Gen Zhu, email: zxg2008vip@163.com Shi-Gang Lu, email: lvshigang1982@sina.com Keywords: BANCR, long non-coding RNA, gastrointestinal cancer, biomarker, meta-analysis Received: October 20, 2016 Accepted: December 13, 2016 Published: December 21, 2016 ABSTRACT BRAF activated non-coding RNA (BANCR) is often dysregulated in cancer. We performed a meta-analysis to clarify its functions as a prognostic indicator in malignant tumors. We searched the PubMed, Medline, OVID, Cochrane Library, and Web of Science databases to identify BANCR-related studies. Nine original studies and 898 total patients were included in the meta-analysis. Hazard ratios (HR) and 95% confidence intervals (CI) were extracted from the included studies to determine the relationship between BANCR expression and patient overall survival (OS). Odds ratios (OR) were calculated using RevMan 5.3 software to assess associations between BANCR expression and pathological parameters. High BANCR expression correlated with lymph node metastasis (LNM) (OR = 3.41, 95% CI: 1.82–6.37, P = 0.0001), distant metastasis (DM) (OR = 2.98, 95% CI: 1.76–5.07, P < 0.0001), tumor stage (OR = 3.11, 95% CI: 1.89–5.12, Z = 3.25, P < 0.0001), and poor OS (pooled HR = 1.98, 95% CI: 1.20–3.27, P = 0.008) in gastrointestinal (GI) cancer patients, but not in non-GI cancer patients. Our results support the notion that BANCR as a promising prognostic biomarker in Chinese patients with GI cancer.
SNORD47 is a member of the C/D box small nucleolar RNAs, which have been implicated in cancer development. We intended to investigate the therapeutic potential of SNORD47 in glioma. We found that the expression of SNORD47 was downregulated in glioma tissues samples and inversely associated with advanced tumor stage (WHO grade IV). Kaplan-Meier survival analysis revealed that glioma patients with high SNORD47 expression had longer overall survival than those with low SNORD47 expression. SNORD47 suppressed the proliferation of glioma cells and induced G2 phase arrest. In addition, upregulation of SNORD47 suppressed invasion and epithelial-mesenchymal transition in glioma cells, and combination treatment with lenti-SNORD47 could augment the anti-tumor effect of temozolomide. These results showed that SNORD47 acted as a tumor suppressor in glioma, and provided the potential anti-tumor function in glioma treatment.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)