MiR-155-5p affects Wilms' tumor cell proliferation and apoptosis via targeting CREB1.

The article "MiR-155-5p affects Wilms' tumor cell proliferation and apoptosis via targeting CREB1", by X.-S. Zhao, B. Han, J.-X. Zhao, N. Tao, C.-Y. Dong, published in Eur Rev Med Pharmacol Sci 2019; 23 (3): 1030-1037-DOI: 10.26355/eurrev_201902_16990-PMID: 30779069, has been retracted by the authors due to a slight deviation in the data. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/16990.

Long noncoding RNA MIAT acts as an oncogene in Wilms' tumor through regulation of DGCR8.

The article "Long noncoding RNA MIAT acts as an oncogene in Wilms' tumor through regulation of DGCR8, by X.-S. Zhao, N. Tao, C. Zhang, C.-M. Gong, C.-Y. Dong, published in Eur Rev Med Pharmacol Sci 2019; 23 (23): 10257-10263-DOI: 10.26355/eurrev_201912_19663-PMID: 31841180" has been withdrawn from the authors due to inaccuracies in the data. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19663#:~:text=CONCLUSIONS%3A%20The%20above%20results%20suggested,and%20therapy%20of%20Wilms'%20tumor.

Long noncoding RNA SNHG16 acts as an oncogene in Wilms' tumor through sponging miR-200a-3p.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA SNHG16 acts as an oncogene in Wilms' tumor through sponging miR-200a-3p, by X.-S. Zhao, N. Tao, C. Zhang, C.-M. Gong, C.-Y. Dong, published in Eur Rev Med Pharmacol Sci 2020; 24 (8): 4145-4151-DOI: 10.26355/eurrev_202004_20994-PMID: 32373950" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/20994.

Long noncoding RNA SNHG16 acts as an oncogene in Wilms' tumor through sponging miR-200a-3p.

OBJECTIVE: Recently, the role of long noncoding RNA (lncRNAs) in tumor progression has attracted much attention. The aim of this study was to investigate the role of lncRNA SNHG16 in the development of Wilms' tumor, and to explore the underlying mechanism. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was used to detect SNHG16 expression in Wilms' tumor patients' tissues. Function assays, including wound healing assay, and transwell assay, were conducted to detect the changes of biological behaviors in Wilms' tumor cells due to gain or loss of SNHG16. Besides, the luciferase reporter gene assay was performed to explore the underlying mechanism. RESULTS: The expression level of SNHG16 was significantly up-regulated in Wilms' tumor tissues when compared with adjacent tissues. Cell migration and invasion abilities were significantly repressed via down-regulation of SNHG16. However, opposite results were obtained after up-regulation of SNHG16 in vitro. After the down-regulation of SNHG16, the expression of miR-200a-3p increased significantly. However, the expression of miR-200a-3p was remarkably reduced via up-regulation of SNHG16 in vitro. Furthermore, SNHG16 acted as a competing endogenous RNA via sponging miR-200a-3p in Wilms' tumor. CONCLUSIONS: SNHG16 induced the metastasis of Wilms' tumor via sponging miR-200a-3p. Our findings might provide a new prospect for the diagnosis and therapy of Wilms' tumor.

MiR-30b-5p and miR-22-3p restrain the fibrogenesis of post-myocardial infarction in mice via targeting PTAFR.

OBJECTIVE: Cardiac fibrosis of post-myocardial infarction (MI) is a precipitating factor of diverse cardiac diseases. MicroRNAs (miRNAs) have been reported to be implicated in the progression of cardiac fibrosis, but the functions and mechanisms of miR-30b-5p and miR-22-3p remain to be investigated. MATERIALS AND METHODS: Cardiac fibroblasts (CFs) were isolated form mice hearts and treated with Angiotensin II (Ang II) for establishing the cardiac fibrosis model of post-MI. The expression of miRNA and mRNA was examined through quantitative real-time polymerase chain reaction (qRT-PCR). Associated protein levels were measured by Western blot. Cell viability was detected via cell counting kit-8 (CCK-8) assay. Dual-Luciferase reporter assay was administered to analyze the target correlation. RESULTS: The down-regulation of miR-30b-5p and miR-22-3p while the up-regulation of platelet activating factor receptor (PTAFR) were found in Ang II-treated CFs. Cell proliferation and collagen deposition were refrained by miR-30b-5p and miR-22-3p overexpression and knockdown of PTAFR. MiR-30b-5p and miR-22-3p directly targeted PTAFR. MiR-30b-5p and miR-22-3p inhibitors alleviated the effects on Ang II-treated CFs induced by PTAFR knockdown through promoting PTAFR. CONCLUSIONS: MiR-30b-5p and miR-22-3p exerted the suppression of fibrogenesis in Ang II-treated CFs via targeting PTAFR, insinuating the indicative roles of miR-30b-5p and miR-22-3p in the fibrogenesis process.

Long noncoding RNA MIAT acts as an oncogene in Wilms' tumor through regulation of DGCR8.

OBJECTIVE: Recent researches have proved that long noncoding RNAs (lncRNAs) cover an important role in malignant tumors. Our study showed how lncRNA myocardial infarction-associated transcript (MIAT) functions in the development of Wilms' tumor. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect the MIAT expression in Wilms' tumor patients. The MIAT expression level and the patients' overall survival time were analyzed. Then, we conducted functional experiments to identify the changes in the biological behaviors of Wilms' tumor cells due to the loss of MIAT. Moreover, further experiments were performed to explore the potential mechanism. RESULTS: By comparing with MIAT expression in adjacent tissues, the MIAT expression level was significantly higher in Wilms' tumor samples. Moreover, the cell growth ability of Wilms' tumor cells was inhibited due to the loss of MIAT. The migrated and invaded ability of the Wilms' tumor cells was inhibited due to the loss of MIAT. Furthermore, the expression of DGCR8 was downregulated due to the loss of MIAT. In addition, it was found that the DGCR8 expression was positively correlated to MIAT expression in Wilms' tumor tissues. CONCLUSIONS: The above results suggested that MIAT could promote the cell proliferation and the metastasis of Wilms' tumor by upregulating DGCR8, which indicated that MIAT might be a potential target for the diagnosis and therapy of Wilms' tumor.

MiR-155-5p affects Wilms' tumor cell proliferation and apoptosis via targeting CREB1.

OBJECTIVE: The aim of this study was to explore the role of microRNA-155-5p (miR-155-5p) in regulating the proliferation and apoptosis of Wilm's tumor (WT), and to investigate the possible underlying mechanism. PATIENTS AND METHODS: The expression levels of miR-155-5p in 37 pairs of WT clinical samples, as well as WT cell line (G401), were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay and flow cytometry assay were used to detect the effects of miR-155-5p on cell proliferation, cycle and apoptosis. Target gene prediction software was applied to screen the potential downstream target gene of miR-155-5p. QRT-PCR, Western blot (WB) and luciferase reporter gene assay proved that cAMP-response element binding protein 1 (CREB1) was the target gene of miR-155-5p. Besides, rescue experiment was conducted to further explore the effect of CREB1 on WT cells. RESULTS: The expression levels of miR-155-5p in WT tissues and cells were both significantly down-regulated. Importantly, miR-155-5p was found to be involved in the malignant behavior of WT cells. MTT assay and flow cytometry assay demonstrated that miR-155-5p significantly inhibited the proliferation, caused stagnation of cells in G0/G1 phase, and promoted cell apoptosis. CREB1 was verified as a functional target gene of miR-155-5p, which was negatively regulated by miR-155-5p. Rescue experiments indicated that restoring the expression of CREB1 could interfere with the effects of miR-155-5p on WT cells. CONCLUSIONS: MiR-155-5p could regulate the proliferation, cell cycle and apoptosis of WT cells. These effects were achieved by regulating the expression of CREB1. Furthermore, our study might provide a new theoretical basis for the basic research of WT.

Establishment of plasma microRNA detection method by using taqman probe based quantitative reverse transcription PCR.

MicroRNAs (miRNAs) are a kind of short non—coding RNAs that regulate gene expression at the post—transcriptional level. Recently, many studies have found that circulating miRNAs have the potential to sever as diagnostic biomarkers for many diseases. However, the methods for the quantification of circulating miRNAs still need more adjustment. In this study, we tried to establish a reliable method to quantify the plasma miRNAs. We used quantitative real—time PCR with taqman probes to detect the plasma miR—153 level. Three controls were used in this study, including two external miRNAs control from C. elegans miRNAs (cel—miR—54 and cel—miR—238) and one internal control (hsa—miR—486). All of these controls were stable in plasma and the cel—miR—238/cel—miR—54/hsa—miR—486 combination could improve the normalization process. The expression level of the target miRNA, human plasma miR—153, could be quantified accurately with taqman probes .The assay has high accuracy, high sensitivity and a large dynamic range from 100 copies to 10(13) copies in the PCR reaction. Our study provided a standardized quantification method for plasma miRNAs which might be used as biomarker in many diseases research.

NRC-interacting factor directs neurite outgrowth in an activity-dependent manner.

Nuclear hormone receptor coregulator-interacting factor 1 (NIF-1) is a zinc finger nuclear protein that was initially identified to enhance nuclear hormone receptor transcription via its interaction with nuclear hormone receptor coregulator (NRC). NIF-1 may regulate gene transcription either by modulating general transcriptional machinery or remodeling chromatin structure through interactions with specific protein partners. We previously reported that the cytoplasmic/nuclear localization of NIF-1 is regulated by the neuronal Cdk5 activator p35, suggesting potential neuronal functions for NIF-1. The present study reveals that NIF-1 plays critical roles in regulating neuronal morphogenesis at early stages. NIF-1 was prominently expressed in the nuclei of developing rat cortical neurons. Knockdown of NIF-1 expression attenuated both neurite outgrowth in cultured cortical neurons and retinoic acid (RA)-treated Neuro-2a neuroblastoma cells. Furthermore, activity-induced Ca(2+) influx, which is critical for neuronal morphogenesis, stimulated the nuclear localization of NIF-1 in cortical neurons. Suppression of NIF-1 expression reduced the up-regulation of neuronal activity-dependent gene transcription. These findings collectively suggest that NIF-1 directs neuronal morphogenesis during early developmental stages through modulating activity-dependent gene transcription.

Wilms' tumor gene 1 expression: an independent acute leukemia prognostic indicator following allogeneic hematopoietic SCT.

To evaluate the prognostic significance of Wilms' tumor gene 1 (WT1) expression for monitoring minimal residual disease and predicting relapse in patients with acute leukemia (AL) following allogeneic hematopoietic SCT (allo-HSCT), the WT1 expression levels of 138 AL patients were measured using real-time quantitative reverse transcription PCR at designed time points after allo-HSCT. All patients were divided into four groups based on the HSCT outcomes and intervention application. A low level of WT1 expression following HSCT indicated a low risk of relapse, whereas WT1 expression >1.05% was indicative of a higher probability of relapse. Only the advanced stage of disease (hazard ratio (HR)=2.73; 95% confidence interval (CI)=1.337-5.573, P=0.006) and a WT1 expression ≥ 0.60% (HR=4.774; 95% CI=2.410-9.459, P=0.000) were associated with lower disease-free survival. Relapse (HR=0.119; 95% CI=0.056-0.250, P=0.000) and a WT1 expression 0.60% (HR=2.771; 95% CI=1.316-5.834, P=0.007) were associated with lower OS. In conclusion, the WT1 expression level is an independent prognostic factor that can predict clinical outcomes for AL patients after HSCT and provide a guide for suitable interventions.

Fabrication and Characterization of a New Self-Assembled Monolayer of Fullerene Dicarboxylic Acid Derivative and Its Photoelectric Conversion Property.

A new fullerene self-assembled monolayer (SAM) which has the property of photoelectric conversion is reported here. The SAM was fabricated on hydrophilic substrates by an esterification reaction. The SAM is characterized by contact angle, AFM, UV spectrum, and cyclic voltammetry. A cathodic photocurrent of 226 nA/cm(2) was obtained. Copyright 2000 Academic Press.