[Retracted] Downregulation of microRNA­198 suppresses cell proliferation and invasion in retinoblastoma by directly targeting PTEN.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the data shown for the cell invasion assays in Figs. 2C and 4C 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: 595­602, 2018; DOI: 10.3892/mmr.2018.8979].

Downregulation of microRNA­198 suppresses cell proliferation and invasion in retinoblastoma by directly targeting PTEN.

A number of studies have highlighted that aberrantly expressed microRNAs (miRNAs/miRs) serve crucial roles in the tumorigenesis and tumor development of retinoblastoma (RB). Hence, a full investigation of the biological roles and regulatory mechanisms of miRNAs in RB may provide novel therapeutic targets for patients with this malignancy. miR­198 is frequently abnormally expressed in various types of human cancers. However, the expression level, biological roles and underlying mechanisms of miR­198 in RB remain to be elucidated. In the present study, miR­198 expression was upregulated in RB tissues and cell lines. Silencing of miR­198 attenuated cell proliferation and invasion in RB. In addition, phosphatase and tensin homolog deleted on chromosome ten (PTEN) was predicted as a potential target of miR­198 using bioinformatics analysis. Subsequent luciferase reporter assay indicated that the 3'­untranslated region of PTEN can be directly targeted by miR­198. Furthermore, miR­198 inhibition increased the PTEN expression at the mRNA and protein levels in RB cells. In addition, PTEN mRNA expression was downregulated in RB tissues, and this downregulation was inversely associated with the expression level of miR­198. PTEN knockdown rescued the inhibitory effects of miR­198 underexpression on cell proliferation and invasion in RB. Notably, the downregulation of miR­198 inactivated the phosphoinositide 3­kinase (PI3K)/protein kinase B (AKT) signaling pathway in RB. These results demonstrated that miR­198 may serve oncogenic roles in RB by directly targeting PTEN and regulating the PI3K/AKT signaling pathway. Hence, miR­198 may be a promising therapeutic target for patients with RB.