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Zhang Z.,Nanchang University | Huang L.,Jiangxi Maternal and Child Health Hospital | Yu Z.,Nanchang University | Chen X.,Nanchang University | And 6 more authors.
DNA and Cell Biology | Year: 2014

MicroRNAs play an important role in the development and progression of Ewing's sarcoma (ES). Especially, the expression of let-7a has been reported to be significantly downregulated in various cancers, and can affect the initiation and maintenance of tumor progression. However, the relative effects of let-7a on ES cells and relative mechanisms are largely unknown. In this study, we identified the underexpression of let-7a in human ES cells comparing with the human mesenchymal stem cells. Then, we sought to compensate for its loss through exogenous transfection with let-7a mimic into ES cell lines A673 and SK-ES-1. Restored let-7a expression inhibited cell proliferation, migration, as well as invasion; arrested cell cycle progression; and induced cell apoptosis of both cell lines. Moreover, bioinformatic prediction suggested that cyclin-dependent kinase 6 (CDK6), which is overexpressed and functions as an oncoprotein in ES cells, is a putative target gene of let-7a. Using mRNA and protein expression analysis and luciferase assays, we further identified the target role of CDK6. Finally, we found that restored CDK6 expression in ES cells that had been treated with let-7a mimic before could partly dampen let-7a-mediated tumor suppression. Taken together, our results showed that let-7a acted as a tumor suppressor in ES by targeting CDK6, and it may provide novel diagnostic and therapeutic options for human Ewing sarcoma clinical operation in future. © Copyright 2014, Mary Ann Liebert, Inc. 2014.


Cao Q.,Key Laboratory of Molecular Medicine of Jiangxi Province | Cao Q.,Nanchang University | Cao Q.,Cardiovascular Systematic Key Laboratory of Jiangxi Province | Li Y.-Y.,Nanchang University | And 7 more authors.
Physiological Genomics | Year: 2013

MicroRNAs (miRNAs, also miR) are a class of noncoding endogenous RNAs that regulate gene expression through binding to protein-coding messenger RNA (mRNA) molecules, predominantly within the 3′-untranslated region (3′-UTR). Signal transducer and activator of transcription 3 (STAT3) is a transcription factor that regulates a battery of genes involved in regulating a variety of biological processes. There is a growing body of evidence demonstrating that miRNAs are closely associated with the STAT3 signaling pathway. In this review, we focus on interactions between miRNAs and the STAT3 signaling pathway, focusing on their reciprocal regulation and roles in cancer. For instance, several papers independently support the existence of regulatory feedback loops between miRNAs and the STAT3 pathway in different cancer contexts including IL-6-STAT3-miR-24/miR-629-HNF4α-miR-124 and IL-6R-STAT3-NF-κB-Lin-28-let-7a. Furthermore, several miRNA components are reported to be involved in STAT3-mediated tumorigenesis, for example miR-21, miR-155, and miR-181b. Through binding to STAT3-binding sites within the promoters of these oncomiRs, STAT3 activates their transcription and mediates tumorigenesis. Some miRNAs directly modulate STAT3 activity through targeting the STAT3 3′-UTR; other miRNAs target SOCS, PIAS3, and EGFR genes, which encode proteins that regulate the STAT3 signaling pathway. Given that miRNAs represent a newly discovered class of regulatory molecules, investigating their biological functions and contribution to pathologies caused by STAT3 dysregulation is essential to improve our understanding of tumorigenesis and to develop novel anticancer therapeutics. The more we can learn about miRNAs-STAT3 interactions, the better able we will be to manipulate them for developing cancer therapeutics. © 2013 the American Physiological Society.


Cai Q.-C.,Sun Yat Sen University | Liao H.,Jiangxi Maternal and Child Health Hospital | Lin S.-X.,Sun Yat Sen University | Xia Y.,Sun Yat Sen University | And 5 more authors.
Medical Oncology | Year: 2012

Diffuse large B-cell lymphoma (DLBCL) is characterized by its clinical and biological heterogeneity. Although the International Prognostic Index (IPI) provides a clinical model for risk stratification of patients with DLBCL, notable variability in outcome is still observed within the same IPI category. Tumor-infiltrating macrophages (also called Tumor-associated macrophages) are the major component in the microenvironment of DLBCL. Their correlation with the prognosis of DLBCL remains controversial. Using a CD68 antibody in immunohistochemical analysis, we studied the expression of CD68 in 112 Chinese patients with DLBCL, with 65 patients (58%) categorized as low CD68 expression and 47 patients (42%) as high CD68 expression. The complete response (CR) rate of patients with low CD68 expression was higher than that with high CD68 expression (66.1% vs. 51.6%), but there was no statistical significance (P = 0.060). The median survival time of patients with low CD68 expression was not achieved and that of high expression was 41 months (P = 0.029). The results suggest that higher expression of CD68 tended to yield poor treatment outcome of DLBCL. © 2011 Springer Science+Business Media, LLC.


Li M.,Northwest University, China | Li M.,Key Laboratory of Plant Nutrition and the Agri environment in Northwest China | Li L.,Jiangxi Normal University | Xu J.,Jiangxi Maternal and Child Health Hospital
Fresenius Environmental Bulletin | Year: 2015

Microcystis aeruginosa was axenically cultured in culture media with varying DIC concentrations (0, 0.2, 0.5,1, 5, 10 m mol L-1, respectively) to test the hypothesis that high level of DIC can stimulate the EPS production and induce colony formation of Microcystis. At the 4th day, the cellular EPS content and cells per particle in the treatments with 0.2,0.5 and 1 m mol L-1 DIC was significantly higher than that in the control sample (without DIC addition). The differences in cellular EPS content and cells per particle among different growth phases were also significant under these conditions. However, it was not expected that the highest level of DIC did not result in the highest cellular EPS content nor obvious colony formation of Microcystis. Our results also showed that the value of cells per particle was almost 1 while EPS content increased from 0.07 pg cell-1 to 0.20 pg cell-1. When the EPS content was higher than 0.20 pg cell-1, the value of cells per particle increased dramatically. This result suggested that the recognized positive linear relationship between colony size and cellular EPS content appeared unless the cellular EPS content was higher than a critical value. © by PSP.


Li Y.,Nanchang University | Zhang Z.,Nanchang University | Liu X.,Nanchang University | Liu X.,Key Laboratory of Molecular Medicine of Jiangxi Province | And 12 more authors.
Molecular and Cellular Biochemistry | Year: 2014

MicroRNAs (miRNAs) play an important role in the development and progression of endometrial carcinoma (EC). Recently, several studies have shown that microRNA-124 (miR-124) is downregulated in various cancers, which can affect tumor initiation and maintenance. However, the effects of miR-124 on EC are largely unknown. In this study, we identified the under-expression of miR-124 in 35 paired EC tissues and adjacent normal tissues. Further, functional experiments found that ectopic expression of miR-124 markedly suppressed cell proliferation, migration, and invasion of EC cells. It also induced cell apoptosis and G1-phase cell cycle arrest. Moreover, we identified signal transducer and activator of transcription 3 (STAT3) as a direct target of miR-124, and over expression of miR-124 not only induced changes in STAT3 expression but also altered expression of its target genes, cyclin D2 and matrix metalloproteinase 2, in the human endometrial carcinoma cell line HEC-1B. In addition to targeting STAT3 directly, we found that miR-124 suppresses phosphorylation of STAT3 through targeting IL-6R indirectly. Restored STAT3 expression through treatment with IL-6 cytokine partly abolished miR-124-mediated cell cycle arrest and apoptosis induction. These results combined with the tumorigenetic role of STAT3 in HEC-1B cells suggest that the antitumor effects of miR-124 are achieved, at least partly, through down regulation of STAT3 mRNA and its downstream target genes. Therefore, inhibition of constitutively activated STAT3 by ectopic expression of miR-124 in EC may provide a novel therapeutic strategy for the treatment of EC. © 2013 Springer Science+Business Media New York.

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