[Corrigendum] MicroRNA-375 inhibits glioma cell proliferation and migration by downregulating RWDD3 in vitro.

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 miR­375 mi + .pCDNA/RWDD3 and miR­375 mi + .pCDNA experiments for the U87 cell line). The authors were able to re­examine 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].

[Retracted] MicroRNA-375 inhibits glioma cell proliferation and migration by downregulating RWDD3 in vitro.

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].

MicroRNA-375 inhibits glioma cell proliferation and migration by downregulating RWDD3 in vitro.

Derived from brain glial cells, gliomas are currently the most common primary tumours in the central nervous system and are characterised by a high recurrence rate and poor prognosis. RWDD3 (RWD domain-containing sumoylation enhancer, also termed RSUME), which can be induced by cellular stress, such as CoCl2, heat shock and hypoxia, may play a crucial role in tumour angiogenesis, growth and metastasis. MicroRNAs (miRNAs) have been demonstrated to act as negative regulators of post-transcriptional gene expression and are involved in tumour growth and metastasis. In the present study, we explored the role of RWDD3 in glioma cell proliferation and invasion by the knockdown of RWDD3 with lentiviral shRNA and demonstrated that miRNA hsa-miR-375, regulates RWDD3 and has an important role in glioma progression. We found that expression of RWDD3 in high-grade gliomas was significantly higher than that noted in normal brain tissues and lower-grade gliomas in vivo. Knockdown of RWDD3 effectively led to cell cycle arrest, decreased proliferation and invasion, and increased apoptosis in human glioma cell lines. Furthermore, miR-375 was downregulated in human gliomas and overexpression of miR-375 caused downregulation of RWDD3 in glioma cells as well as inhibited their motility. Thus, these findings suggest that RWDD3 and miR-375 may function as therapeutic biomarkers for glioma patients.

Long noncoding RNA activated by TGF-ß in human cancers: A meta-analysis.

BACKGROUND: Because long non-coding RNA ATB (activated by TGF-ß) is dysregulated in many cancers, we performed a meta-analysis to determine its prognostic potential in malignant tumors. METHODS: We searched electronic databases, including PubMed, Medline, OVID, Cochrane Library and Web of Science from inception until November 15, 2016 and identified eight studies with 818 cancer patients for the meta-analysis. We analyzed the hazard ratios (HRs) and 95% confidence intervals (CIs) to determine the relationship between lncRNA-ATB expression and overall survival (OS), recurrence -free survival (RFS), disease-free survival (DFS). We also use RevMan5.3 software to calculate odds ratio (ORs) to assess the association between lncRNA-ATB expression and pathological parameters including lymph node metastasis (LNM), distant metastasis (DM) and tumor stage. RESULTS: Our analysis showed that increased lncRNA-ATB expression was associated with OS (HR=2.82, 95% CI:1.98-4.00, P<0.00001), DFS (HR=2.75, 95% CI:1.73-4.38, P<0.0001), RFS(HR=3.96, 95% CI:2.30-6.81, P<0.00001), LNM (OR=4.07, 95% CI 1.74-9.53, P=0.001), DM (OR=3.21, 95% CI 1.06-9.72, P=0.04) and high tumor stage (OR=2.81, 95% 1.78-4.43, P<0.0001) in patients with other types of cancers that excluded pancreatic cancer. CONCLUSIONS: Meta-analysis demonstrated that increased lncRNA-ATB expression can be a useful prognostic biomarker in human cancer.

Long noncoding RNA CCAT2 can predict metastasis and poor prognosis: A meta-analysis.

BACKGROUND: It has been reported that Colon cancer-associated transcript 2 (CCAT2) is dysregulated in various cancers. We performed this meta-analysis to clarify its promising functions as a prognosis marker in malignant tumors. METHODS: Electronic databases, including PubMed, Medline, OVID, Cochrane Library, and Web of Science, were searched from inception to October 20, 2016. The hazard ratio (HR) and 95% confidence interval (CI) were calculated to explore the relationship between CCAT2 expression and survival, which were extracted from the eligible studies. The odds ratio (OR) was calculated to assess the association between CCAT2 expression and pathological parameters using RevMan5.3 software. RESULTS: Six original studies were included in this meta-analysis including 725 cancer patients. The pooled HR suggested that high CCAT2 expression was significantly correlated with overall survival (OS) (HR=2.30, 95% CI: 1.62-3.25, p<0.00001) in cancer patients. Subgroup analysis revealed a significant association between CCAT2 and OS in urogenital system (HR=1.70, 95% CI: 1.27-2.26, p<0.003) and non-urogenital system cancer patients (HR=3.18, 95% CI: 2.09-4.83, p<0.0001). A significant association was observed between high CCAT2 expression and poor progression-free survival (PFS) in cancer patients (pooled HR=2.76, 95% CI: 1.74-4.37). CCAT2 expression was significantly related to lymph node metastasis (LNM) (OR=4.33, 95% CI 2.03-9.22), distant metastasis (DM) (OR=11.66, 95% CI: 5.36-25.37) and tumor stage (OR=2.58, 95% CI 1.86-3.57). CONCLUSIONS: This meta-analysis demonstrated that high CCAT2 expression significantly predicts poor OS, poor PFS, LNM, DM and tumor stage, suggesting that high CCAT2 expression may serve as a novel biomarker for poor prognosis and metastasis in cancers.