[Retracted] microRNA­574 inhibits cell proliferation and invasion in glioblastoma multiforme by directly targeting zinc finger E­box­binding homeobox 1.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the data shown in the cell invasion assays in Figs. 2C and 5C were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 18: 1826­1834, 2018; DOI: 10.3892/mmr.2018.9106].

microRNA­574 inhibits cell proliferation and invasion in glioblastoma multiforme by directly targeting zinc finger E­box­binding homeobox 1.

Accumulated evidence has demonstrated that dysregulation of microRNAs (miRNAs) contributes to tumourigenesis and tumour development of glioblastoma multiforme (GBM). Therefore, miRNAs may be promising candidates in the development of prognosis biomarkers and effective therapeutic targets for patients with GBM. A number of studies have reported that miRNA­574 (miR­574) is aberrantly expressed in multiple types of human cancers. However, the expression pattern, biological functions and molecular mechanism of miR­574 in GBM are yet to be elucidated. Therefore, the present study aimed to determine the expression level and biological functions of miR­574 in GBM and the underlying molecular mechanisms. In the present study, miR­574 levels were measured by reverse transcription­quantitative polymerase chain reaction (RT­qPCR) and were demonstrated to be significantly downregulated in human GBM tissues and cell lines. Functional experiments indicated that restored expression of miR­574 using mimics led to the inhibition of the cell proliferation and invasion of GBM cells, as determined by Cell Counting kit­8 and Matrigel invasion assays, respectively. In addition, bioinformatics analysis predicted that zinc finger E­box­binding homeobox 1 (ZEB1) may be a target of miR­574. Subsequent RT­qPCR, western blot analysis and luciferase reporter assays confirmed that ZEB1 was a direct target of miR­574 in GBM. Additionally, ZEB1 was demonstrated to be upregulated and inversely correlated with miR­574 expression in clinical GBM tissues. Rescue experiments demonstrated that overexpression of ZEB1 attenuated the inhibitory effects of miR­574 on the proliferation and invasion of GBM cells. Overall, the results of the present study highlighted the potential tumour inhibitory roles of miR­574 in GBM, thereby indicating that miR­574 may be a novel and efficient therapeutic target for the treatment of patients with GBM.

Correlation of the expression of miR-146a in peripheral blood mononuclear cells of patients with ankylosing spondylitis and inflammatory factors.

We investigated the expression of miR-146a in peripheral blood mononuclear cell (PBMC) of patients with ankylosing spondylitis (AS) and its correlation with inflammatory factors to explore the clinical significance. In total 45 patients with AS were selected at the Weifang People's Hospital from June, 2014 to January, 2016. At the same time, 30 healthy volunteers were also selected to serve as control group. Expression level of miR-146a in PBMC cells of patients in each group was detected by quantitative real-time-polymerase chain reaction (qRT-PCR). Levels of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and IL-6 in serum and the supernatant of culture medium of PBMC derived from each group were detected by enzyme-linked immunosorbent assay (ELISA). Correlations between expression level of miR-146a and serum inflammatory factors, and clinical indicators were analyzed. Clinical indicators included bath ankylosing spondylitis disease activity index (BASDAI), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and duration of morning stiffness. Expression level of miR-146a in PBMC of AS patients was significantly higher than that of healthy control (P<0.01); levels of TNF-α, IL-1ß and IL-6 in serum and the supernatant of culture medium of PBMC derived from AS patients were significant compared to those of control group (P<0.01); expression of miR-146a in PBMC of patients with AS was positively correlated with the levels of TNF-α, IL-1ß and IL-6 in serum (r=0.632, P<0.01; r=0.574, P<0.01; r=0.483, P<0.01). In addition, expression level of miR-146a in PBMC of patients with AS was positively correlated with BASDAI, ESR, CRP and duration of morning stiffness (r=0.551, P<0.01; r=0.738, P<0.01; r=0.685, P<0.01; r=0.497, P<0.01). Expression level of miR-146a in PBMC of AS patients was significantly increased and the expression level was positively correlated with the levels of TNF-α, IL-1ß and IL-6 in serum (P<0.05). In addition, expression level of miR-146a in PBMC of AS patients was also positively correlated with BASDAI, ESR, CRP and duration of morning stiffness. Those results suggest that miR-146a may be involved in the pathogenesis of AS, and the expression level of miR-146a in PBMC cells may be helpful for diagnosis of AS and judgment of disease activity.