[Retracted] MicroRNA­663 inhibits the proliferation, migration and invasion of glioblastoma cells via targeting TGF­ß1.

Subsequently to the publication of the above article, an interested reader drew to the Editor's attention that they had identified several instances of overlapping data panels comparing between the scratch­wound assay data ('36 h' experiments) portrayed in Figs. 3 and 8; furthermore, there appeared to be an overlap in a pair of the data panels shown for the Transwell assay experiments with U87 cells in Fig. 9 (albeit with an inversion of one of the panels), such that these data may have been derived from the same original source, even though they were purportedly intended to show the results from differently performed experiments. Given the multiple instances of overlapping data panels 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 on account of a lack of overall confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 35: 1125­1134, 2016; DOI: 10.3892/or.2015.4432].

Coiling Is Not Superior to Clipping in Patients with High-Grade Aneurysmal Subarachnoid Hemorrhage: Systematic Review and Meta-Analysis.

BACKGROUND: Outcomes of coiling embolization versus clipping for patients with high-grade aneurysmal subarachnoid hemorrhage (aSAH) have not been previously compared. We reviewed current evidence regarding the safety and efficacy of clipping versus coiling for high-grade aSAH. METHODS: We conducted a meta-analysis of studies that compared clipping with coiling in patients with high-grade aSAH published from January 1999 to February 2016 in Medline, Embase, and Cochrane databases based on PRISMA inclusion and exclusion criteria. Binary outcome comparisons between clipping and coiling were described using odds ratios (ORs). RESULTS: Three randomized controlled trials (RCTs) and 16 observational studies were included. There was no statistical difference in good outcome rates between the clipping and coiling groups (OR, 1.44; 95% confidence interval [CI], 0.97-2.13). Subgroup analysis showed no significant difference between the 2 treatments in non-RCTs (OR, 1.49; 95% CI, 0.95-2.36) and RCTs (OR, 1.15; 95% CI, 0.59-2.25). Coiling was associated with higher mortality (OR, 0.55; 95% CI, 0.41-0.75). Lower mortality was associated with clipping in non-RCTs (OR, 0.54; 95% CI, 0.40-0.74), but there was no difference in the RCTs (OR, 0.79; 95% CI, 0.19-3.39). Coiling was not associated with lower rates of complications including rebleeding (OR, 0.62; 95% CI, 0.30-1.29), ischemic infarct (OR, 0.89; 95% CI, 0.53-1.49), symptomatic vasospasm (OR, 0.76; 95% CI, 0.45-1.29), or shunt-dependent hydrocephalus (OR, 1.33; 95% CI, 0.52-3.40). CONCLUSION: The outcome with coiling is not superior to clipping in patients with high-grade aSAH; moreover, coiling has a greater risk of mortality.

MicroRNA-663 inhibits the proliferation, migration and invasion of glioblastoma cells via targeting TGF-ß1.

Cell migration and invasion are key processes involved during tumor metastasis. Recently, microRNAs (miRs) have been demonstrated to play important roles in the regulation of cancer metastasis. However, the underlying mechanisms remain unknown. Here, we aimed to investigate the exact role of miR-663 in the metastasis of glioblastoma as well as the underlying mechanisms. By performing quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis, we demonstrated that miR-663 was significantly downregulated in glioblastoma tissues (n=25), when compared to that in normal brain tissues (n=15). In addition, its expression levels were also reduced in human glioblastoma cell lines, A172 and U87. Furthermore, restoration of miR-663 expression led to a significant decrease in the cell proliferation, migration and invasion of human glioblastoma A172 and U87 cells. We further identified TGF-ß1 as a direct target of miR-663, and found that the expression of TGF-ß1 was negatively mediated by miR-663 at the post-transcriptional level in glioblastoma cells. Moreover, overexpression of TGF-ß1 significantly reversed the inhibitory effects of miR-663 upregulation on the proliferation, migration and invasion in A172 and U87 cells. In addition, our data suggest that MMP2 and E-cadherin, a key factor in epithelial-mesenchymal transition (EMT), are involved in the miR-633/TGF-ß1-mediated metastasis of glioblastoma. In summary, miR-663 plays an inhibitory role in the regulation of proliferation, migration and invasion of glioblastoma cells, partly at least, via direct mediation of TGF-ß1 as well as downstream MMP2 and E-cadherin. Therefore, we suggest that miR-663 is a potential candidate for the prevention of glioblastoma metastasis.