[Retracted] MicroRNA­936 inhibits the malignant phenotype of retinoblastoma by directly targeting HDAC9 and deactivating the PI3K/AKT pathway.

Following the publication of the above paper, it was drawn to the Editors' attention by a concerned reader that certain of the flow cytometric data featured in Figs. 2D, 4D and 5D, the colony formation assay data shown in Figs. 2C, 4C and 5C, and the tumor images shown in Fig. 7A 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 were already under consideration for publication, or had already been published, prior to its submission to Oncology 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. [Oncology Reports 43: 635­645, 2020; DOI: 10.3892/or.2020.7456].

Knockdown of Long Non-coding RNA TUG1 Suppresses Migration and Tube Formation in High Glucose-Stimulated Human Retinal Microvascular Endothelial Cells by Sponging miRNA-145.

Diabetic retinopathy (DR) is a serious complication of diabetes mellitus. The purpose of this study was to investigate the potential functional role of long non-coding RNA TUG1 in high glucose (HG)-stimulated human retinal microvascular endothelial cells (hRMECs). The results demonstrated that following 72 h of HG stimulation, enhanced proliferation, migration, and tube formation process were observed in hRMECs. Moreover, HG treatment markedly increased TUG1 expression in hRMECs, and knockdown of TUG1 notably restrained the aberrant phenotypes of hRMECs induced by HG. Mechanistically, TUG1 may serve as a competing endogenous RNA (ceRNA) for miR-145, thereby blocking the repression on VEGF-A in hRMECs. Rescue experiments further indicated that inhibition of miR-145 abolished the beneficial role of TUG1 knockdown in HG-treated hRMECs. Our data suggested that knockdown of TUG1 protects hRMECs against HG stimulation partly by regulating miR-145/VEGF-A axis.

MicroRNA­936 inhibits the malignant phenotype of retinoblastoma by directly targeting HDAC9 and deactivating the PI3K/AKT pathway.

MicroRNA­936 (miR­936) has been reported to play important roles in the progression of non­small cell lung cancer and glioma. However, the expression and functions of miR­936 in retinoblastoma (RB) remain elusive and need to be further elucidated. Herein, the aims were to measure miR­936 expression in RB, identify the functional importance of miR­936 in the oncogenicity of RB, and investigate the underlying molecular mechanisms. Reverse­transcription quantitative PCR was carried out to determine miR­936 expression in RB tissues and cell lines. Cell proliferation, colony formation, apoptosis, migration, and invasion in vitro and tumor growth in vivo were examined respectively by Cell Counting Kit­8, colony formation, flow cytometric, and Transwell migration and invasion assays and a subcutaneous heterotopic xenograft experiment. The potential target of miR­936 was predicted by bioinformatic analysis and was subsequently validated by luciferase reporter assay, reverse­transcription quantitative PCR, and western blotting. miR­936 expression was weak in both RB tissues and cell lines and was correlated with differentiation, lymph node metastasis and TNM staging in RB. RB cell proliferation, colony formation, migration, and invasion in vitro and tumor growth in vivo were attenuated by exogenous miR­936, whereas apoptosis was enhanced by miR­936 overexpression. Further molecular investigation identified histone deacetylase 9 (HDAC9) as a direct target gene of miR­936 in RB cells. HDAC9 depletion had effects similar to those of miR­936 overexpression in RB cells. Recovery of HDAC9 expression counteracted the tumor­suppressive action of miR­936 on the oncogenicity of RB cells. Ectopic miR­936 expression deactivated the PI3K/AKT pathway in RB cells in vitro and in vivo by decreasing HDAC9 expression. Downregulated miR­936 is related to poor prognosis in RB, and its upregulation inhibits RB aggressiveness via direct targeting of HDAC9 mRNA and thereby inactivation of the PI3K/AKT pathway.

Systematic variations associated with renal disease uncovered by parallel metabolomics of urine and serum.

BACKGROUND: Membranous nephropathy is an important glomerular disease characterized by podocyte injury and proteinuria, but no metabolomics research was reported as yet. Here, we performed a parallel metabolomics study, based on human urine and serum, to comprehensively profile systematic metabolic variations, identify differential metabolites, and understand the pathogenic mechanism of membranous nephropathy. RESULTS: There were obvious metabolic distinctions between the membranous nephropathy patients with urine protein lower than 3.5 g/24 h (LUPM) and those higher than 3.5 g/24 h (HUPM) by Partial Least Squares Discriminant Analysis (PLS-DA) model analysis. In total, 26 urine metabolites and 9 serum metabolites were identified to account for such differences, and the majority of metabolites were significantly increased in HUPM patients for both urines and serums. Combining the results of urine with serum, all differential metabolites were classified to 5 classes. This classification helps globally probe the systematic metabolic alterations before and after blood flowing through kidney. Citric acid and 4 amino acids were markedly increased only in the serum samples of HUPM patients, implying more impaired filtration function of kidneys of HUPM patients than LUPM patients. The dicarboxylic acids, phenolic acids, and cholesterol were significantly elevated only in urines of HUPM patients, suggesting more severe oxidative attacks than LUPM patients. CONCLUSIONS: Parallel metabolomics of urine and serum revealed the systematic metabolic variations associated with LUPM and HUPM patients, where HUPM patients suffered more severe injury of kidney function and oxidative stresses than LUPM patients. This research exhibited a promising application of parallel metabolomics in renal diseases.

[Dynamic observation of periodontal pathogens and cariogenic bacteria in modified chemostat using confocal laser scanning microscopy].

OBJECTIVE: To study dynamic relation between periodontal pathogens and cariogenic bacteria under analogous oral environment. METHODS: Eight periodontopathic and cariogenic bacteria of Porphyromonas gingivalis (Pg), Actinobacillus actinomycetemcomitans (Aa), Fusobacterium nucleatum (Fn), Provotella intermedium (Pi), Streptococcus mutans (Sm), Streptococcus sanguis (Ss), Actinomyces viscosus (Av) and Lactobacillus acidophilus (La) were used. These eight strains were cultured in modified chemostat under analogous oral environment which contained 600 ml modified BM medium supplemented with 2.5 g/L porcine gastric mucin, respectively. After 1, 24, 48 and 96 h, optical sectioning of plaque biofilms on removable and replaceable hydroxyapatite disks was analyzed by the combination of live bacterial Gram fluorescence staining and confocal laser scanning microscopy. Biofilm thickness and reconstruction of the three-dimensional architecture of plaque biofilms were made. RESULTS: Biofilm thickness increased significantly with time (P < 0.001). Biofilms of Aa were thinner than those of Ss and eight-specie biofilms were thicker than those formed by Ss and Aa per time point. Three-dimensional images showed periodontal pathogens mainly occurred in cariogenic bacterial complex or on the biofilm surface. CONCLUSIONS: Gram-positive cariogenic species initially predominated in artificial plaque, followed by the increasing proportions of Gram-negative periodontal pathogens. The relation between microecological balance among bacteria and diseases is worthy of further studies.