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Zhao Y.,Zhengzhou University | Wang B.,Zhengzhou University | Hu K.,Henan Academy of Medical science | Wang J.,Zhengzhou University | And 5 more authors.
Oncology Letters | Year: 2015

The GSTT1 gene encodes a key enzyme involved in the metabolism of xenobiotics and its polymorphisms have been associated with individual susceptibility to various malignancies. Numerous molecular epidemiological studies have been performed to investigate the association between GSTT1 gene polymorphisms and lung cancer susceptibility; however, the results of previous studies were inconsistent. Therefore, the aim of the present study was to conduct a meta-analysis in order to derive a more precise estimation of the association in the East Asian populations. The meta-analysis included 7,415 lung cancer cases and 6,084 controls from 26 published studies in East Asia, which were selected from the PubMed and China National Knowledge Infrastructure databases, up to March 20, 2014. Using crude odds ratios (ORs) with 95% confidence intervals (CIs), a statistically significant association was identified between the GSTT1 null genotype and lung cancer in the East Asian populations (OR=1.17; 95% CI, 1.09-1.25; Pheterogeneity=0.003). Furthermore, subgroup analyses revealed that the lung cancer risk in smokers carrying the GSTT1 null genotype was significantly increased compared with non-smokers (OR=1.71; 95% CI, 1.04-2.81; Pheterogeneity=0.002). Thus, the GSTT1 null genotype may increase the risk of lung cancer among the East Asian populations © 2015, Spandidos Publications. All Rights Reserved. Source


Liang S.,Zhengzhou University | Liang S.,Henan University of Science and Technology | Jiao H.-L.,Zhengzhou University | Chi L.-K.,Zhengzhou University | And 8 more authors.
Chinese Journal of Tissue Engineering Research | Year: 2013

Background: Wnt signaling pathway is a key to occurrence and development of tumor. Several studies have demonstrated that Dickkopf-1 can block intracellular Wnt signalling transmission. Objective: To investigate the inhibitory effect and underlying mechanism of human umbilical cord mesenchymal stem cells on C6 glioma growth by a co-culture system in vitro. Methods: C6 glioma cells were cultured with human umbilical cord mesenchymal stem cells conditioned medium under different concentrations. Cell Counting Kit-8 and flow cytometry analysis were performed to investigate cell proliferation and cell cycle status. Western blotting was used to detect the expression of β-catenin and c-Myc in C6 cells treated with human umbilical cord mesenchymal stem cells conditioned medium. Enzyme-linked immunosorbent assay was adopted to examine the level of Dickkopf-1 secreted by human umbilical cord mesenchymal stem cells. Dickkopf-1 in human umbilical cord mesenchymal stem cells conditioned medium was neutralized by anti-Dickkopf-1 antibody. The effects of antibody neutralization were also determined by the above methods. Results and Conclusion: Human umbilical cord mesenchymal stem cells could inhibit C6 cell expansion and arrest the cell cycle in G0-G1 phase. The expression levels of β-catenin and c-Myc were down-regulated in C6 cells after treatment with human umbilical cord mesenchymal stem cells conditioned medium. The levels of secreted protein Dickkopf-1 were positively correlated with concentrations of human umbilical cord mesenchymal stem cells conditioned medium. The inhibitory effect of human umbilical cord mesenchymal stem cells on C6 cell proliferation was enhanced as the concentration of Dickkopf-1 in human umbilical cord mesenchymal stem cells conditioned medium increased. When Dickkopf-1 was neutralized by anti-Dickkopf-1 antibody, the suppressing effect was attenuated. It demonstrated that human umbilical cord mesenchymal stem cells could inhibit glioma cell growth via secreting the soluble factors, such as Dickkopf-1. Source


Wang G.,Henan University of Science and Technology | Zeng G.,Henan University of Science and Technology | Wang C.,Henan University of Science and Technology | Wang H.,Zhengzhou University | And 4 more authors.
Biomedical Papers | Year: 2015

Background and Aim. Amniotic membrane-derived mesenchymal stem cells (hAM-dMSCs) are a potential source of mesenchymal stem cells which could be used to repair skin damage. The use of mesenchymal stem cells to repair skin damage requires safe, effective and biocompatible agents to evaluate the effectiveness of the result. Quantum dots (QDs) composed of CdSe/ZnS are semiconductor nanocrystals with broad excitation and narrow emission spectra, which have been considered as a new chemical and fluorescent substance for non-invasively labeling different cells in vitro and in vivo. This study investigated the cytotoxic effects of QDs on hAM-dMSCs at different times following labeling. Methods. Using 0.75, 1.5 and 3.0 μL between quantum dots, labeled human amniotic mesenchymal stem cells were collected on days 1, 2 and 4 and observed morphological changes, performed an MTT cell growth assay and flow cytometry for mesenchymal stem cells molecular markers. Results. Quantum dot concentration 0.75 μg/mL labeled under a fluorescence microscope, cell morphology was observed, The MTT assay showed cells in the proliferative phase. Flow cytometry expression CD29, CD31, CD34, CD44, CD90, CD105 and CD106. Conclusions. Within a certain range of concentrations between quantum dots labeled human amniotic mesenchymal stem cells has good biocompatibility. © 2015 PALACKY UNIV. All rights reserved. Source


Wang Y.,Henan Academy of Medical science | Dai Y.,Zhengzhou University | Li X.,Zhengzhou University | Chen C.,Zhengzhou University | And 2 more authors.
Acta Biologica Hungarica | Year: 2011

The effect of all-trans retinoic acid (atRA) on palatal fusion and the underlying mechanisms were investigated using organ culture. Compared with control group, the atRA-treated group (1 μM and 5 μM) had more medial edge epithelium (ME) remaining within the midline epithelial seam (MES). At 10 μM atRA, the opposing shelves were not in contact at the culture end (72 h). Cell death detection by TUNEL and laminin immunohistochemistry demonstrated that atRA (5 μM) induced apoptosis in mesenchyme and inhibited degradation of basal lamina within MES. Notably, migration and apoptosis of ME cells and degradation of basal lamina within MES markedly represented vehicle control palatal shelves in culture. Additionally, apoptosis was not detected in mesenchyme of control palatal shelves. Immunoblotting analysis revealed that Smad2 and Smad3 were endogenously activated and expression of Smad7 was inhibited during the fusion process. In contrast, atRA treatment abrogated phosphorylation of Smad2 and Smad3 and inducible expression of Smad7 in ME. From these data, it is assumed that inhibition of Smad pathway by atRA in ME may play a critical role in abrogation of the ME cell apoptosis and degradation of the basal laminin, which might contribute to failure of palatal fusion. © 2011 Akadé miai Kiadó, Budapest. Source


Ma S.,Zhengzhou University | Liang S.,Zhengzhou University | Liang S.,Henan University of Science and Technology | Jiao H.,Zhengzhou University | And 6 more authors.
Molecular and Cellular Biochemistry | Year: 2014

Mesenchymal stem cells (MSCs) represent a potential therapeutic target for glioma. We determined the molecular mechanism of inhibitory effect of human umbilical cord-derived MSCs (hUC-MSCs) on the growth of C6 glioma cells. We demonstrated that hUC-MSCs inhibited C6 cell growth and modulated the cell cycle to G0/G1 phase. The expression of β-catenin and c-Myc was downregulated in C6 cells by conditioned media from hUC-MSCs, and the levels of secreted DKK1 were positively correlated with concentrations of hUCMSCs-CM. The inhibitory effect of hUC-MSCs on C6 cell proliferation was enhanced as the concentration of DKK1 in hUCMSCs-CM increased. When DKK1 was neutralized by anti-DKK1 antibody, the inhibitory effect of hUC-MSCs on C6 cells was attenuated. Furthermore, we found that conditioned media from hUC-MSCs transfection with siRNA targeting DKK1 mRNA or pEGFPN1-DKK1 plasmid lost or enhanced the abilities to regulate the Wnt signaling in C6 cells. Therefore, hUC-MSCs inhibited C6 glioma cell growth via secreting DKK1, an inhibitor of Wnt pathway, may represent a novel therapeutic strategy for malignant glioma. © 2013 Springer Science+Business Media New York. Source

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