[Retracted] MicroRNA­21 promotes migration and invasion of glioma cells via activation of Sox2 and ß­catenin signaling.

Following the publication of the above paper, a concerned reader drew to the Editor's attention that there were several data panels showing the results of Transwell migration and invasion assay experiments in Figs. 1A and 2A that contained overlapping sections of data, such that these data, which were intended to have shown the results from differently performed experiments, appeared to have been derived from a smaller number of original sources. Furthermore, the data panels shown in Fig. 3A for the 'Control/U343' and 'Control/172', and the 'miR­21/ß­catenin' and 'Control/T98', experiments were also found to be unexpectedly similar, given that these were likewise intended to show the results from differently performed experiments. After having conducted an independent investigation in the Editorial Office, the Editor of Molecular Medicine Reports has determined that the above paper should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [Molecular Medicine Reports 15: 187­193, 2017; DOI: 10.3892/mmr.2016.5971].

Preoperative Imaging and Microscopic Navigation During Surgery Can Avoid Unnecessarily Opening the Mastoid Air Cells Through Craniotomy Using the Retrosigmoid Approach.

OBJECTIVE: To analyze treatment of microvascular decompression using the retrosigmoid approach (RA) in primary trigeminal neuralgia and hemifacial spasm using preoperative images combined with intraoperative microscopic navigation to avoid unnecessarily opening the mastoid air cells (MACs). METHODS: Ten patients with primary trigeminal neuralgia and 20 patients with hemifacial spasm (test group) were treated using RA for microvascular decompression. Preoperative head magnetic resonance angiography and temporal bone computed tomography were performed and the images registered using SPM12 and fused with MRIcron to determine the relationship between MACs and sigmoid sinuses. An O-arm was used for navigation, and the transverse sigmoid sinus was projected under a microscope to guide RA. A control group comprised 139 patients who had the same surgical procedure as the test group but without image processing or intraoperative navigation. RESULTS: The relationship between MACs and the ipsilateral sigmoid sinus was classified as follows: I, MACs did not exceed the lateral edge of the ipsilateral sigmoid sinus (10/60); II, MACs exceeded the ipsilateral lateral edge of the sigmoid sinus but did not exceed the medial edge (42/60); and III, MACs exceeded the medial edge of the ipsilateral sigmoid sinus (8/60). Test and control groups showed significant differences in the incidences of opening MACs (P = 0.003). There was no cerebrospinal fluid leakage or scalp and intracranial infection at follow-up. CONCLUSIONS: Image processing and intraoperative microscopic navigation can avoid unnecessarily opening MACs and might reduce postoperative cerebrospinal leakage and scalp infection after RA craniotomy.

miR-135a-5p and miR-124-3p Inhibit Malignancy of Glioblastoma by Downregulation of Syndecan Binding Protein.

Due to its high invasiveness, glioblastoma is difficult to treat by surgery, radiotherapy, chemotherapy or any combination therapy. Syndecan binding protein (SDCBP), a widely distributed intracellular scaffold protein, has an important role in both physiological and pathological process. In the current work, we have identified target sequences for miR-135a-5p and miR-124-3p in the 3'-untranslated region of the SDCBP mRNA. Therefore, we have investigated the relationship between SDCBP, miR-135a-5p and miR-124-3p in glioblastoma multiforme cells T98G and U87 in vitro and in vivo. Dual luciferase activity assay documented that SDCBP is, in fact, the target of miR-135a-5p, miR-124-3. Western blot, qRT-PCR, proliferation, migration, and invasion assays have demonstrated that of silencing SDCBP or overexpressing miR-135a-5p/miR-124-3p significantly interferes with the malignant properties of glioblastoma cells. In vivo studies have shown that silencing SDCBP or overexpressing miR-135a-5p/miR-124-3p result in a marked decrease of tumor size and prolong life of tumor-bearing mice. A therapy combining the three treatments inhibits synergistically subcutaneous tumor growth in nude mice. In conclusion, proliferation, migration and invasion of glioblastoma can be inhibited by targeted regulation of SDCBP through upregulation of miR-135a-5p and miR-124-3p.

MicroRNA­21 promotes migration and invasion of glioma cells via activation of Sox2 and ß­catenin signaling.

The expression of microRNA 21 (miR-21) has been reported to be upregulated in various types of cancer, including malignant gliomas. However, its functions and mechanisms in glioma remain to be fully elucidated. The present study established miRNA­21 overexpression and knockdown cell lines using SRY­box 2 (Sox2) small interfering RNA (siRNA) to knockdown expression and Sox2 cDNA was cloned into pcDNA 3.1 mammalian expression vector for ectopic expression. BIO and XAV­939 were used for ß­catenin signaling activation and knockdown, respectively. Transwell chambers were used to assay the capacity of cells to migrate. The present study determined that increased expression of miR­21 significantly promoted the migration and invasion of glioma cells, which was accompanied by an upregulated expression of the Sox2 protein. Sox2 overexpression also promoted glioma cell migration and invasion, whereas Sox2 siRNA markedly reduced the miR­21­enhanced migration and invasion of glioma cells, indicating Sox2 may act as a crucial mediator of miR­21 function. Furthermore, miR­21 also upregulated the protein expression level of ß­catenin, whereas anti­miR­21 and Sox2 knockdown significantly reduced ß­catenin expression. BIO, a ß­catenin specific agonist, enhanced migration and invasion of glioma cells. XAV­939, an inhibitor of ß­catenin signaling, markedly inhibited the migration and invasion of glioma cells, suggesting that ß­catenin may be associated with miR­21­ and Sox2­induced invasion of glioma cells. Notably, BIO restored the migration and invasion potential of glioma cells, which were inhibited by Sox2 siRNA and anti­miR­21. These findings indicated that ß­catenin may be an important downstream mediator of miR­21 and Sox2. Therefore, the present study identified the miR­21/Sox2/ß­catenin signaling pathway, which may regulate the migration and invasion of human glioma cells.

Co-metabolic degradation of tetrabromobisphenol A by novel strains of Pseudomonas sp. and Streptococcus sp.

Three strains capable of rapidly degrading TBBPA by co-metabolism and utilizing formate as the carbon source, named as J-F-01, J-F-02, and J-F-03, respectively, were isolated from enrichment cultures, which have been treated with 0.5mg/L TBBPA for 240 d. Based on morphology and 16S rRNA gene sequence analysis, both J-F-01 and J-F-02 were determined to Pseudomonas sp., while J-F-03 was identified as Streptococcus sp. A shorter half-life (6.1d) of TBBPA was observed in pure culture of J-F-03 when compared with J-F-01 (22.5d) and J-F-02 (13.6d). Surprisingly, the degradation of TBBPA was significantly enhanced by the mixed culture of J-F-02 and J-F-03. The optimal degradation conditions for the mixed cultures were determined. Under the optimal conditions, TBBPA (0.5mg/L) was completely metabolized by the mixed culture within ten days. Moreover, bromide and the metabolisms were detected, and a possible metabolic pathway was deduced from the detection of metabolite production patterns.

Biodegradation of tetrabromobisphenol A by a novel Comamonas sp. strain, JXS-2-02, isolated from anaerobic sludge.

A bacterial strain able to rapidly degrade tetrabromobisphenol A (TBBPA), JXS-2-02, was isolated from anaerobic sludge that had been successfully enrichment by adding TBBPA for 240 days. JXS-2-02 can use TBBPA as the sole carbon and energy source for growth in mineral salt medium. Based on morphology, biochemical characteristics and 16S rDNA sequence analysis, JXS-2-02 was identified as Comamonas sp.. Under the optimal conditions (pH 7.0, a temperature of 30 °C and an inoculum of 1% OD(600) = 0.6), more than 86% of the initial TBBPA (0.5 mg L(-1)) was degraded after 10d. A TBBPA biodegradation pathway was proposed on the basis of the metabolite production patterns and the identification of the metabolites by GC-MS analysis. This study is the first report to isolate a single TBBPA-degrading bacterial strain under anaerobic conditions for TBBPA debromination and detoxification.

Social isolation produces anxiety-like behaviors and changes PSD-95 levels in the forebrain.

Isolation rearing induces profound behavioral and neurochemical abnormalities in rodents. However there have been many controversies with its anxiogenic-like effects using models like elevated-plus maze. In the current study we aimed to address this by using one novelty-based anxiety paradigm that has been largely overlooked in previous isolation rearing studies. We found that eight-week isolation rearing produced potent anxiogenic-like effects in novelty-induced hypophagia test in mice. We also demonstrated PSD-95 levels were elevated in the hippocampus and amygdala and reduced in the frontal cortex after social isolation. This study provides further behavioral and neurochemical evidence to support that isolation rearing can produce anxiogenic-like effects in rodents.

Autophagy inhibition promotes gambogic acid-induced suppression of growth and apoptosis in glioblastoma cells.

OBJECTIVE: To investigate the effects of gambogic acid (GA) on the growth of human malignant glioma cells. METHODS: U251MG and U87MG human glioma cell lines were treated with GA and growth and proliferation were investigated by MTT and colony formation assays. Cell apoptosis was analyzed by annexin V FITC/PI flow cytometry, mitochondrial membrane potential assays and DAPI nuclear staining. Monodansylcadaverine (MDC) staining and GFP-LC3 localisation were used to detect autophagy. Western blotting was used to investigate the molecular changes that occurred in the course of GA treatment. RESULTS: GA treatment significantly suppressed cell proliferation and colony formation, induced apoptosis in U251 and U87MG glioblastoma cells in a time- and dose-dependent manner. GA treatment also lead to the accumulation of monodansylcadaverine (MDC) in autophagic vacuoles, upregulated expressions of Atg5, Beclin 1 and LC3-II, and the increase of punctate fluorescent signals in glioblastoma cells pre-transfected with GFP-tagged LC3 plasmid. After the combination treatment of autophagy inhitors and GA, GA mediated growth inhibition and apoptotic cell death was further potentiated. CONCLUSION: Our results suggested that autophagic responses play roles as a self-protective mechanism in GA-treated glioblastoma cells, and autophagy inhibition could be a novel adjunctive strategy for enhancing chemotherapeutic effect of GA as an anti-malignant glioma agent.

Global mapping of ZBTB7A transcription factor binding sites in HepG2 cells.

ZBTB7A is a known proto-oncogene that is implicated in carcinogenesis and cell differentiation and development. Fully understanding the function of ZBTB7A in cellular processes could provide useful strategies for cancer treatment and development-associated disease therapy. Here, global mapping of ZBTB7A transcription factor binding sites was developed by utilizing microarray technology in HepG2 cells. The data obtained from the microarrays was further validated via chromatin immunoprecipitation-PCR (ChIP-PCR) and real time-PCR, and it was revealed that ZBTB7A may be one of the regulators of neural development. ZBTB7A target signal pathways were identified in signal pathway and GO (Gene Ontology) analyses. This is the first report on the global mapping of ZBTB7A downstream direct targets, and these findings will be useful in understanding the roles of ZBTB7A in cellular processes.