Weight gain promotes the progression of IgA nephropathy in Asians: A protocol for systematic review and meta-analysis.

INTRODUCTION: The relationship between weight gain and progression of IgA nephropathy (IgAN) has been investigated by many researchers but remains controversial. The incidence of IgAN is significantly higher in Asia than in other regions. Therefore, we investigated the relationship between weight gain and primary IgAN in the Asian population. METHODS AND ANALYSIS: Seven databases were retrieved up to now. We stratified the included population by body mass index (BMI) and performed a meta-analysis of associated risk factors. OBJECTIVES: In this study, Asian IgAN patients with different BMI were grouped together to clarify the relationship between BMI and IgAN progression in Asian populations, so as to provide more ideas and treatment means for the prevention and treatment of IgAN in the future.

[Retracted] MicroRNA­22 functions as a tumor suppressor by targeting SIRT1 in renal cell carcinoma.

Following the publication of this paper, the authors have contacted the Editorial Office to explain that they are unable to reproduce the results of various of their experiments after having repeated some of them, and consequently they wish to retract the paper.owing to a lack of confidence in the presented data. It was also drawn to the attention of the Office that certain of the tumor images shown in Fig. 6A were strikingly similar to data appearing in different form in other articles by different authors. Considering all these points, the Editor of Oncology Reports is in agreement that this paper should be retracted from the Journal. The authors all agree with the decision to retract this paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 35: 559­567, 2016; DOI: 10.3892/or.2015.4333].

MicroRNA-22 functions as a tumor suppressor by targeting SIRT1 in renal cell carcinoma.

Accumulating evidence demonstrates that microRNA-22 (miR-22) was deregulated in many types of cancers and was involved in various cellular processes related to carcinogenesis. However, the exact roles and mechanisms of miR-22 remain unknown in human renal cell carcinoma (RCC). Here, the relationship between miR-22 expression pattern and clinicopathological features of patients with EOC were determined by real-time quantitative RT-PCR (qRT-PCR). Furthermore, the role of miR-22 and possible molecular mechanisms in EOC were investigated by several in vitro approaches and in a nude mouse model. Results from qRT-PCR showed that miR-22 was significantly downregulated in RCC samples compared with corresponding non-cancerous tissues, which was significantly associated with tumor stage and lymph node metastasis. Functional study demonstrated that enforced overexpression of miR-22 in renal cancer cells inhibited proliferation, migration and invasion, and induced cell apoptosis in vitro, and suppressed tumor growth in vivo. In addition, SIRT1 was identified as a direct target of miR-22 by a luciferase reporter assay. Overexpression of miR-22 activated p53 and its downstream target p21 and PUMA, and the apoptosis markers cleaved CASP3 and PARP, and inhibited epithelial-mesenchymal transition (EMT). These findings showed that miR-22 functioned as tumor suppressor in RCC and blocked RCC growth and metastasis by directly targeting SIRT1 in RCC, indicating a potential novel therapeutic role in RCC treatment.