[Retracted] miR­148a suppresses human renal cell carcinoma malignancy by targeting AKT2.

Following the publication of the above paper, an interested reader drew to our attention that the western blot data shown in Fig. 7, the scratch­wound assay data in Fig. 2D and the cell invasion assay data in Fig. 2E were strikingly similar to data that had already been published in different articles by different authors from different research institutions, or which were already under consideration for publication elsewhere. Independently of the reader's enquiry, the authors contacted the Editorial Office to request that the paper be retracted on account of the fact that they were unable to reproduce the results presented in Fig. 2. Owing to the fact that the contentious data in the above article were already under consideration for publication, or had already been published, elsewhere when it was submitted to Oncology Reports, and in line with the authors' own request, the Editor has decided that this paper should be retracted from the Journal. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 37: 147­154, 2017; DOI: 10.3892/or.2016.5257].

miR-148a suppresses human renal cell carcinoma malignancy by targeting AKT2.

MicroRNA-148a (miR-148a) has been reported to be deregulated in different tumor types, whereas the biological function of miR-148a in renal cell carcinoma (RCC) largely remains unexplored. In the present study we investigated the clinical significance, biological effects, and the underlying molecular mechanisms of miR-148 in RCC. Here, we showed that miR-148a was significantly downregulated in RCC tissues and cell lines. Low expression of miR-148a in RCC tissues was associated with large tumor size, advanced TNM stage, and lymph node metastasis. Functional assays revealed that overexpression of miR-148a significantly inhibited RCC cell proliferation, colony formation, migration and invasion in vitro and suppressed RCC xenograft tumor growth in vivo. In addition, using quantitative RT-PCR (qRT-PCR), western blot analysis and luciferase reporter assays, AKT2 was confirmed to be a direct target of miR-148a. AKT2 expression was upregulated, and was negatively correlated with miR-148a expression in RCC tissues (r=-0.641, P<0.001). Silencing of AKT2 phenotypically copied miR-148a-induced phenotypes, whereas re-expression of AKT2 reversed the suppressive effects of miR-148a in RCC cells. Further mechanistic investigations showed that miR-148a exerted its antitumor activity via inhibition of the AKT pathway in vitro and in vivo. Taken together, these findings suggest that miR-148a functions as tumor suppressor in RCC by targeting AKT2.