[Retracted] 14­3­3ß exerts glioma­promoting effects and is associated with malignant progression and poor prognosis in patients with glioma.

[This retracts the article DOI: 10.3892/etm.2017.5664.].

[Retracted] Knockdown of PREX2a inhibits the malignant phenotype of glioma cells.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that cell invasion assay data in the article (featured in Fig. 4A) were strikingly similar to data appearing in different form in another article by different authors at different research institutions, which had already been published elsewhere at the time of the present article's submission. Furthermore, flow cytometric data featured in Fig. 2D were strikingly similar to those in another previously published paper, and cell cyle data included in Fig. 3 had apparently previously published elsewhere. Owing to the fact that the contentious data in the above article had already appeared in different form in other articles prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors also expressed their intention to retract the paper on the grounds that the corresponding author and several of the authors failed to confirm the approval of the final version of the manuscript. The Editor apologizes to the readership for any inconvenience caused. [the original article was published on Molecular Medicine Reports 13: 2301­2307, 2016; DOI: 10.3892/mmr.2016.4799].

14-3-3ß exerts glioma-promoting effects and is associated with malignant progression and poor prognosis in patients with glioma.

Glioma is a type of tumor that affects the central nervous system. It has been demonstrated that 14-3-3ß, a protein that is mainly concentrated in the brain, serves an important role in tumor regulation. However, the mechanism of action of 14-3-3ß that underlies the pathogenesis of glioma remains to be elucidated. In the present study, 14-3-3ß was silenced by RNA interference in the human glioma cell line U373-MG. Following knockdown of 14-3-3ß, the proliferation, colony formation, cell cycle progression, migration and invasion of U373-MG cells were significantly decreased (P<0.01), whereas cell apoptosis was increased (P<0.01). Furthermore, in a tumor xenograft experiment, silencing 14-3-3ß significantly inhibited the in vivo tumor growth of U373-MG cells (P<0.01). The results demonstrated that 14-3-3ß levels were significantly higher in human glioma tissues compared with normal brain tissues (P<0.01) and high 14-3-3ß expression was significantly associated with advanced pathological grade (P<0.03) and low Karnofsky performance scale (P<0.003). Patients with glioma who had high 14-3-3ß levels had a significantly shorter survival time compared with those with low expression of 14-3-3ß (P=0.031), suggesting that 14-3-3ß may be an effective predictor of the prognosis of patients with glioma. The results of the present study indicate that 14-3-3ß serves an oncogenic role in glioma, suggesting that 14-3-3ß may have potential as a promising therapeutic target for glioma.

Knockdown of PREX2a inhibits the malignant phenotype of glioma cells.

Glioma is the most common type of malignant brain tumor. Phosphatidylinositol­3,4,5­trisphosphate­dependent Rac exchange factor 2a (PREX2a), which is a regulator of the small guanosine triphosphatase Rac, has previously been identified as an oncoprotein that inhibits phosphatase and tensin homolog deleted on chromosome 10 (PTEN) activity. However, the role of PREX2a in the regulation of the malignant phenotype of glioma has yet to be reported. The present study demonstrated that the mRNA and protein expression levels of PREX2a were significantly increased in glioma tissue, as compared with in normal brain tissue. Furthermore, the expression levels of PREX2a were positively correlated with tumor grade. PREX2a­specific small interfering RNA­mediated knockdown significantly inhibited proliferation and induced apoptosis of SWO­38 glioma cells. Furthermore, inhibition of PREX2a expression significantly suppressed cell cycle progression in glioma cells, as detected by cell cycle arrest at G1 phase. In addition, knockdown of PREX2a inhibited the invasion of SWO­38 glioma cells. The present study also investigated the molecular mechanisms underlying the effects of PREX2a knockdown, and demonstrated that phosphoinositide 3­kinase signaling was significantly downregulated, which may be due to the upregulation of PTEN activity. In conclusion, the present study is the first, to the best of our knowledge, to suggest that knockdown of PREX2a may effectively inhibit the malignant phenotype of glioma in vitro; therefore, PREX2a may be considered a potential molecular target for the treatment of glioma.