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Zhu Y.,Second Hospital of Jiaxing | Xiao X.,First Peoples Hospital of Kunshan | Dong L.,Second Hospital of Jiaxing | Liu Z.,Guangxi Medical University
Tumor Biology | Year: 2012

MicroRNAs are small noncoding RNA molecules that control the expression of target genes. Our previous studies show that let-7a decreased in gastric carcinoma and that up-regulation of let-7a by gene augmentation inhibited gastric carcinoma cell growth both in vitro and in vivo, whereas it remains largely unclear as to how let-7a affects tumor growth. In this study, proteins associated with the function of let-7a were detected in high-throughput screening. The cell line of SGC-7901 stably overexpressing let-7a was successfully established by gene clone. Two-dimensional gel electrophoresis (2-DE) was used to separate the total proteins of SGC-7901/let-7a, SGC-7901/EV and SGC-7901, and PDQuest software was applied to analyze 2-DE images. Ten differential protein spots were identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry, and they may be the proteins associated with let-7a function. The overexpressed proteins include antioxidant protein 2, insulin-like growth factor binding protein 2, protein disulfide isomerase A2, C-1-tetrahydrofolate synthase, cyclin-dependent kinase inhibitor1 (CDKN1) and Rho-GTPase activating protein 4. The underexpressed proteins consisted of S-phase kinase-associated protein 2 (Spk2), platelet membrane glycoprotein, fibronectin and Cks1 protein. Furthermore, the different expression levels of the partial proteins (CDKN1,Spk2 and Fibronectin) were confirmed by Western blot analysis. The data suggest that these differential proteins are involved in novel let-7a signal pathway, and these findings provided the basis to comprehensively investigate the functional mechanisms of let-7a in gastric carcinoma. © 2012 International Society of Oncology and BioMarkers (ISOBM). Source


Zhu Y.,Second Hospital of Jiaxing | Xiao X.,First Peoples Hospital of Kunshan | Dong L.,Second Hospital of Jiaxing | Liu Z.,Guangxi Medical University
Analytical Cellular Pathology | Year: 2012

MicroRNAs are small noncoding RNA molecules that control expression of target genes. Our previous studies show that let-7a decreased in gastric carcinoma and that up-regulation of let-7a by gene augmentation inhibited gastric carcinoma cell growth both in vitro and in vivo, whereas it remains largely unclear as to how let-7a affects tumor growth. In this study, proteins associated with the function of let-7a were detected by high throughout screening. The cell line of SGC-7901 stablely overexpressing let-7a was successfully established by gene cloning. Two-dimensional gel electrophoresis (2-DEy was used to separate the total proteins of SGC-7901/let-7a, SGC-7901/EV and SGC-7901, and PDQuest software was applied to analyze 2-DE images. Ten different protein spots were identified by MALDI-TOF-MS, and they may be the proteins associated with let-7a function. The overexpressed proteins included Antioxidant protein 2, Insulin-like growth factor binding protein 2, Protein disulfide isomerase A2, C-1-tetrahydrofolate synthase, Cyclin-dependent kinase inhibitor1 (CDKN1) and Rho-GTPase activating protein 4. The underexpressed proteins consisted of S-phase kinase-associated protein 2 (Spk2), Platelet membrane glycoprotein, Fibronectin and Cks1 protein. Furthermore, the different expression levels of the partial proteins (CDKN1, Spk2 and Fibronectin) were confirmed by western blot analysis. The data suggest that these differential proteins are involved in a novel let-7a signal pathway and these findings provide the basis to investigate the functional mechanisms of let-7a in gastric carcinoma. © 2012 - IOS Press and the authors. All rights reserved. Source


Yao J.,Nanjing Medical University | Jiang M.,First Peoples Hospital of Kunshan | Zhang Y.,Nanjing Medical University | Liu X.,Nanjing Medical University | And 2 more authors.
International Immunopharmacology | Year: 2016

Asthma is a chronic airway inflammatory disorder and progresses mainly due to airway remodeling. Chrysin, a natural flavonoid, has been reported to possess multiple biologic activities, including anti-inflammation, anti-oxidation and anti-proliferation. The present study aimed to investigate whether chrysin could relieve allergic airway inflammation and remodeling in a murine model of chronic asthma and the mechanism involved. The female BALB/c mice sensitized and challenged with ovalbumin (OVA) successfully developed airway hyperresponsiveness (AHR), inflammation and remodeling. The experimental data showed that chrysin could alleviate OVA-induced AHR. Chrysin could also reduce OVA-induced increases in the number of inflammatory cells, especially eosinophils, interleukin (IL) -4, and IL-13 in bronchoalveolar lavage fluid (BALF) and total IgE in serum. The decreased interferon-γ (IFN-γ) level in BALF was also upregulated by chrysin. In addition, inflammatory cell infiltration, goblet cell hyperplasia and the expression of α-smooth muscle actin (α-SMA) around bronchioles were suppressed by chrysin. Furthermore, the phosphorylation levels of Akt and extracellular signal-regulated kinase (ERK) could be decreased by chrysin, which are associated with airway smooth muscle cell (ASMC) proliferation. These results indicate the promising therapeutic effect of chrysin on chronic asthma, especially the progression of airway remodeling. © 2016 Elsevier B.V. All rights reserved. Source


Wang H.-G.,Nanjing Medical University | Huang X.-D.,Nanjing Medical University | Shen P.,Nanjing Medical University | Li L.-R.,Nanjing Medical University | And 2 more authors.
International Journal of Molecular Medicine | Year: 2013

In the present study, we investigated the anticancer effects of sodium butyrate (NaBu) on hepatocellular carcinoma (HCC) cells in vitro. As a histone deacetylase (HDAC) inhibitor, NaBu upregulated Ac-H3 and inhibited HDAC4 protein expression in a time- and dose-dependent manner. MTT assays showed that treatment with NaBu at high concentrations significantly inhibited the growth of various HCC cells. Exposure to NaBu for 24 h induced cell cycle arrest in the SMMC-7721 and HepG2 cells. NaBu also induced the apoptosis of SMMC 7721 cells. The expression levels of cell cycle- and apoptosis-related proteins were further investigated by western blot analysis using specific antibodies. The results provided a possible mechanism responsible for the inhibitory effects of NaBu on the growth of HCC cells. To further analyze the role of NaBu in cell migration, wound healing and Transwell assays were performed, indicating that NaBu significantly inhibits cell migration/invasion in HCC cells. Transforming growth factor-β1 (TGF-β1)-induced epithelial to mesenchymal transition (EMT) has been associated with tumor cell migration and invasion. The EMT markers, E-cadherin, vimentin and N-cadherin, were regulated by TGF-β1, while NaBu inhibited this process in which HDAC4 and matrix metalloproteinase (MMP)7 may be involved. Based on our findings, we propose that NaBu may be useful as an anticancer drug for HCC therapy. Copyright © 2013 Spandidos Publications Ltd. Source


Yan W.,Nanjing Medical University | Qian C.,Nanjing Medical University | Zhao P.,Nanjing Medical University | Zhang J.,Nanjing Medical University | And 7 more authors.
Neuro-Oncology | Year: 2010

Osteopontin (OPN) is widely overexpressed in various cancers, including gliomas, and plays an important role in tumorigenesis. However, the expression pattern and functions of OPN splice variants expressed in gliomas remain unclear. The aims of our current study were to examine the expression pattern and functions of OPN splice variants in gliomas. In present study, the mRNA levels of OPN splice variants are markedly increased in gliomas tissues, and all OPN splice variants were also found in U251 and U87 cells. Furthermore, knock-down and regain of function experiments were designed to explore the functions of OPN splice variants in U251 and U87 cells. Lentiviral vectors of OPN small interference RNA (siRNA) targeting all three endogenous mRNAs of OPN and OPN splice variants synonymous mutant that were not silenced by OPN siRNA were constructed. Our results showed that all OPN splice variants synonymous mutant-protected glioma cells from apoptosis induced by OPN siRNA through alteration of the levels of Bcl-2 family proteins and OPN-b Mu elicted a significant effect. Both OPN-a Mu and -c Mu promoted glioma cell invasion through alteration of the levels of uPA, MMP-2, and MMP-9 expressions and the activities of MMP-2 and MMP-9 via activation PI-3K/AKT/NF-κB signaling pathway. Moreover, OPN-c Mu showed the strongest effect on glioma cell invasion, while OPN-b Mu showed no effect on the invasion of U251 and U87 cells. Thus, different splice variants of OPN have divergent functions in regulating apoptosis and invasion of glioma cells, which broadens their importance in glioma biotherapy. © The Author(s) 2010. Source

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