Ming Zhou

The Third Xiangya Hospital of the Central South University, Ch’ang-sha-shih, Hunan, China

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Publications (85)171.49 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Human SPLUNC1 can suppress NPC tumor formation, however, the correlation between SPLUNC1expression and NPC patient prognosis has not been reported. In this study, we used a large-scale sample of 1,015 tissue cores to detect SPLUNC1 expression and its association with patient prognosis. SPLUNC1 expression was reduced in NPC samples compared to non-tumor nasopharyngeal epithelial (NPE) tissues. Positive expression of SPLUNC1 in NPC predicted a better prognosis (Disease Free Survival (DFS): P=0.034, Overall Survival (OS): P=0.048). Cox's Proportional Hazards Model revealed that SPLUNC1 could be a significant prognostic factor affecting DFS (P=0.027). A cDNA microarray analyzed by SAM and IPA revealed that an indirect interaction existed between SPLUNC1 and retinoic acid (RA) in the cancer regulatory network. To further investigate the molecular mechanisms involved, we utilized several bioinformatics tools and identified 12 retinoid X receptors (RXRs) heterodimer binding sites in the promoter region of the SPLUNC1 gene. The transcriptional activity of the SPLUNC1 promoter was up-regulated significantly by all-trans-retinoic acid (ATRA). SPLUNC1 and RA receptor expression were induced significantly by ATRA, and removal of ATRA led to a progressive loss of SPLUNC1 and RA receptor expression. ATRA inhibited proliferation and induced the differentiation of NPC cells. Interestingly, over-expression of SPLUNC1 sensitized NPC cells to ATRA, whereas knockdown of SPLUNC1 in HNE1 cells increased cell viability. Under SPLUNC1 knockdown conditions, differentiation was reversed with ATRA treatment. We concluded that SPLUNC1 could potentially predict prognosis for NPC patients and play an important role in ATRA-induced growth inhibition and differentiation in NPC cells.This article is protected by copyright. All rights reserved.
    FEBS Journal 08/2014; · 4.25 Impact Factor
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    ABSTRACT: Nasopharyngeal carcinoma (NPC) is a major head and neck cancer with high occurrence in Southeast Asia and southern China. To identify novel biomarkers for the early detection of NPC patients, 2D-DIGE combined with MALDI-TOF-MS analysis was performed to identify differentially expressed proteins in the carcinogenesis and progression of NPC using LCM-purified normal nasopharyngeal epithelial tissues and various stages of NPC biopsies. As a result, 26 differentially expressed proteins were identified, of which two proteins with sharp expressional changes in the carcinogenic process, ENO1 and CYPA, were validated by western blot analysis and identified as critical seed proteins in the functional network. Immunohistochemistry assay was further performed to detect the expression of the two proteins with a tissue microarray that included various stages of NPC tissues. The ability of these proteins to detect NPC early was evaluated via a receiver operating characteristic analysis. The results indicated that the combination of the two proteins could perfectly discriminate NNET and AH from stage I of NPC with high sensitivity and specificity, which is more effective than using either of the two proteins individually. In summary, the combination of ENO1 and CYPA can serve as potential molecular markers for the early detection of NPC.
    Journal of proteomics. 07/2014;
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    ABSTRACT: In this paper we synthesize well aligned Ni–Co sulfide nanowire arrays (NWAs) with a Ni–Co molar ratio of 1:1 on 3D nickel foam by a facile two-step hydrothermal method. Owing to the low electronegativity of sulfur, Ni–Co sulfide NWAs exhibit a more flexible structure and much higher conductivity compared with Ni–Co oxide NWAs when used as active materials in supercapacitors. The electrochemistry tests show that these self-supported electrodes are able to deliver ultrahigh specific capacitance (2415 F g−1 and 1176 F g−1 at a current density of 2.5 mA cm−2 and 30 mA cm−2, respectively), together with a considerable areal capacitance (6.0 F cm−2 and 2.94 F cm−2 at a current density of 2.5 mA cm−2 and 30 mA cm−2, respectively), and good rate capability. More importantly, the asymmetric supercapacitor, composed of Ni–Co sulfide NWAs as the positive electrode and activated carbon as the negative electrode, reaches up to an energy density of 25 W h kg−1 and a power density of 3.57 kW kg−1 under a cell voltage of 1.8 V. Furthermore, the two assembled supercapacitors in series can power a 3 mm diameter red (2.0 V, 20 mA) round light-emitting diode (LED) indicator for more than 30 minutes after charging separately for a total time of 6 min. The superior electrochemistry capacity demonstrates that the self-standing Ni–Co sulfide nanowire arrays are promising for high-performance supercapacitor applications.
    J. Mater. Chem. A. 04/2014; 2(18).
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    ABSTRACT: Density functional theory based calculations have been employed to investigate structures and properties of coupled tetragonal pyramid (CTP) Pt7 based Pt(7-x)Nix (x=1, 2, 3) bimetallic clusters, and the reaction mechanism of methanol dehydrogenation to CO on Pt7 and PtNi bimetallic clusters. The models chosen to catalyze the methanol are Pt7 (CTP, quintet) cluster and Pt5Ni2 (I) cluster (two Pt atoms in the bottom of Pt7 (CTP) are replaced by Ni atoms) which is the most stable structure among all the isomers of Pt(7-x)Nix (x=1, 2, 3). The methanol dehydrogenation on Pt7 (CTP) cluster preferentially proceeds along the pathway of CH3OH→ CH2OH→CH2O→CHO→CO, while on Pt5Ni2 (І) the pathway of CH3OH→CH3O→CH2O→ CHO→CO is more favorable. In addition, the complete dehydrogenation product of methanol, CO, can more easily dissociate from Pt5Ni2 (I) than that on Pt7. Electronic configuration analysis shows that charge transfer from Ni to Pt and results in increase of the electron density in Pt 5d orbitals. Moreover, the density of states (DOS) at Fermi level of clusters reduces gradually as the increase of the doped Ni atoms and this improves the catalytic activity for methanol decomposition.
    Computational and Theoretical Chemistry. 01/2014;
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    ABSTRACT: Nonresolving inflammatory processes affect all stages of carcinogenesis. Lactoferrin, a member of the transferrin family, is involved in the innate immune response and anti-inflammatory, anti-microbial, and anti-tumor activities. We previously found that lactoferrin is significantly down-regulated in specimens of nasopharyngeal carcinoma (NPC) and negatively associated with tumor progression, metastasis, and prognosis of patients with NPC. Additionally, lactoferrin expression levels are decreased in colorectal cancer as compared with normal tissue. Lactoferrin levels are also increased in the various phases of inflammation and dysplasia in an azoxymethane-dextran sulfate sodium (AOM-DSS) model of colitis-associated colon cancer (CAC). We thus hypothesized that the anti-inflammatory function of lactoferrin may contribute to its anti-tumor activity. Here we generated a new Lactoferrin knockout mouse model in which the mice are fertile, develop normally, and display no gross morphological abnormalities. We then challenged these mice with chemically induced intestinal inflammation to investigate the role of lactoferrin in inflammation and cancer development. Lactoferrin knockout mice demonstrated a great susceptibility to inflammation-induced colorectal dysplasia, and this characteristic may be related to inhibition of NF-κB and AKT/mTOR signaling as well as regulation of cell apoptosis and proliferation. Our results suggest that the protective roles of lactoferrin in colorectal mucosal immunity and inflammation-related malignant transformation, along with a deficiency in certain components of the innate immune system, may lead to serious consequences under conditions of inflammatory insult.
    PLoS ONE 01/2014; 9(7):e103298. · 3.73 Impact Factor
  • Applied Surface Science 01/2014; 315:81–89. · 2.54 Impact Factor
  • Acta Biochimica et Biophysica Sinica 12/2013; · 1.81 Impact Factor
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    ABSTRACT: MiRNAs can function as oncogenes or tumor suppressor genes. The abnormal expression of miRNAs leads to tumor malignant phenotypes, such as cell proliferation, apoptosis, invasion and metastasis, through which it is involved in the process of tumor initiation, progression and transcriptional regulation network. Therefore, it is important to clarify the mechanism of miRNA involved in the process of tumor initiation and progression. MiRNA regulation mechanism in tumor initiation and progression includes one-to-many and many-to-one regulation between TFto- miRNA and miRNA-to-target gene, which increases the complexity of miRNA regulation, thus affecting the biological behavior of the tumor, The expression and activity of Drosha and Dicer in the process of miRNA affect the synthesis of mature miRNA and involve in the process of tumor initiation and progression; ceRNA may bind with miRNA by competing with miRNA targeting genes and affect biological function of miRNA as miRNA inhibitor. Therefore the abnormal expression and structure of ceRNA is an important molecular mechanism of tumor initiation and progression. This complicated regulation network comprised by multi-dimensional regulation model and specific regulation of tumor initiation and progression provides impetus to exploring the functional restoration of miRNA as a novel target for cancer diagnosis and therapy.
    Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences 12/2013; 38(12):1282-1288.
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    ABSTRACT: Glioma is a common and lethal type of brain tumor. Serum peptides reflected the pathological changes of body. Here we studied the serum peptide profiles to distinguish glioma disease and measure glioma staging. Serum peptides were captured by WCX magnetic beads and were analyzed by MALDI-TOF mass spectrometer. Sera from 53 glioma patients and 69 age-matched healthy controls were analyzed. Clinpro Tools software was used to obtain a common peak m/z list from all measured samples. An optimal subset of peptides was selected to establish predictive classification model with the newly developed competitive adaptive reweighted sampling (CARS) variable selection method and serum peptide profiles was classified through a partial least-squares-linear discriminate analysis (PLS-LDA). We also searched for peptide peaks with progressively different that correlated with increasing malignancy of glioma. The following pattern recognition equation was established with selected peptide signals: Y=-0.1113-0.113X1-0.2916X2+0.1128X3-0.2057X4-0.2047X5-0.3048X6+0.2835X7+0.3121X8-0.1458X9+0.0354X10-0.2022X11. Using this pattern, classification sensitivity and specificity achieved 0.9057 and 0.9855, respectively. Additionally, we detected 3 peptide signals that correlated with glioma grade. Among these, the intensity of peak 2082.32Da correlated positively with glioma progressing, and peaks with size of 3316.08Da and 6631.45Da shown decreasing intensity with increasing glioma grade. 11-peptide recognition pattern and specific peak intensities might be useful for the early detection and tumor staging of glioma, but they need further validate and evaluate in independently clinical settings.
    Clinica chimica acta; international journal of clinical chemistry 08/2013; · 2.54 Impact Factor
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    ABSTRACT: Glioblastoma is the most common type of primary brain tumors. Cisplatin is a commonly used chemotherapeutic agent for Glioblastoma patients. Despite a consistent rate of initial responses, cisplatin treatment often develops chemoresistance, leading to therapeutic failure. Cellular resistance to cisplatin is of great concern and understanding the molecular mechanisms is an utter need. Glioblastoma cell line U251 cells were exposed to increasing doses of cisplatin for 6 months to establish cisplatin-resistant cell line U251R. The differential miRNA expression profiles in U251 and U251R cell lines were identified by microarray analysis and confirmed by Q-PCR. MiRNA mimics were transfected into U251R cells, and cellular response to cisplatin-induced apoptosis and cell cycle distribution were examined by FACS analysis. U251R cells showed 3.1-fold increase in cisplatin resistance compared to its parental U251 cells. Microarray analysis identified Let-7b and other miRNAs significantly down-regulated in U251R cells compared to U251 cells. Transfection of Let-7b mimics greatly re-sensitized U251R cells to cisplatin, while transfection of other miRNAs has no effect or slightly effect. Cyclin D1 is predicted as a target of Let-7b through bioinformatics analysis. Over-expression of Let-7b mimics suppressed cyclin D1 protein expression and inhibited cyclin D1-3'-UTR luciferase activity. Knockdown of cyclin D1 expression significantly increased cisplatin-induced G1 arrest and apoptosis. Collectively, our results indicated that cisplatin treatment leads to Let-7b suppression, which in turn up-regulates cyclin D1 expression. Let-7b may serve as a marker of cisplatin resistance, and can enhance the therapeutic benefit of cisplatin in glioblastoma cells.
    Journal of Experimental & Clinical Cancer Research 06/2013; 32(1):41. · 3.07 Impact Factor
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    ABSTRACT: The link between nonresolving inflammation and cancer is well documented. On the one hand, epidemiologic evidence supports that approximately 25% of all human cancer worldwide is caused by nonresolving inflammation. On the other hand, inflammatory cells are found in the microenvironment of most, if not all, tumors. In the tumor micro-environment, inflammatory cells and molecules influence almost every aspect of cancer. MicroRNAs (miRNAs) participate in the initiation and progression of nonresolving inflammation-related cancer by regulating the key genes and related signaling pathways. Further investigation into the molecular mechanisms by which miRNAs carry out their functions will be of great value in the prevention, early diagnosis, and treatment of tumors.
    Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences 06/2013; 38(6):639-644.
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    ABSTRACT: LTF (lactotransferrin, or lactoferrin) plays important role in innate immunity, and its anti-tumor function has also been reported in multiple cancers. We previously reported that LTF is significantly down-regulated in nasopharyngeal carcinoma (NPC) and acts as a tumor suppressor by suppressing AKT signaling. However, the exact mechanism of the down-regulation of LTF in NPC has not been revealed. In the current study, we screened and identified LTF is a bona fide target of miR-214 in NPC cells. miR-214 mimics significantly suppressed LTF mRNA and protein expression levels in NPC cells. miR-214 not only can promote NPC cell proliferation and invasion abilities in vitro, but also can accelerate tumor formation and lung metastasis in a mouse xenograft model. The pro-tumor function of miR-214 was depended on LTF suppression since LTF re-expression can reverse it. miR-214 can also activate AKT signaling by suppressing LTF expression. Furthermore, miR-214 expression level was up-regulated in NPC especially in metastasis-prone NPC tumor tissues compared with normal nasopharyngeal epithelial tissues, while the LTF expression level was negatively correlated with miR-214, suggesting that miR-214 targeting is partly responsible for LTF down-regulation in NPC specimens.
    Tumor Biology 03/2013; · 2.52 Impact Factor
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    ABSTRACT: Long-palate, lung and nasal epithelium clone 1 (LPLUNC1) gene expression is relatively tissue specific. It is highly expressed in nontumor nasopharyngeal epithelial tissues, but its expression is reduced in nasopharyngeal carcinoma (NPC), indicating that LPLUNC1 may be associated with the tumorigenesis of NPC. To study the effects of LPLUNC1 on NPC tumorigenesis, a full-length LPLUNC1 expression plasmid was stably transfected into the NPC cell line, 5-8F. Our data indicated that LPLUNC1 inhibited NPC cell proliferation in vitro and tumor formation in vivo. LPLUNC1 also delayed cell cycle progression from G1 to S phase and inhibited the expression of cyclin D1, cyclin-dependent kinase 4 (CDK4) and phosphorylated Rb. To further investigate the molecular mechanisms underlying the suppressive effects of LPLUNC1 on NPC tumorigenesis, cDNA microarray was performed. These studies revealed that LPLUNC1 inhibited the expression of certain mitogen-activated protein (MAP) kinases (MAPK) kinases and cell cycle-related molecules. Western blotting confirmed that the expression of MEK1, phosphorylated ERK1/2, phosphorylated JNK1/2, c-Myc and c-Jun were inhibited by LPLUNC1. Furthermore, the transcriptional activity of AP-1 was down-regulated by LPLUNC1, suggesting that the MAPK signaling pathway is regulated by LPLUNC1. Taken together, the present study indicates that LPLUNC1 delays NPC cell growth by inhibiting the MAPK and cyclin D1/E2F pathways and suggests that LPLUNC1 may represent a promising candidate tumor suppressor gene associated with NPC.
    PLoS ONE 01/2013; 8(5):e62869. · 3.73 Impact Factor
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    ABSTRACT: Little is known about the role of the host defensive protein short palate, lung and nasal epithelium clone 1 (SPLUNC1) in the carcinogenesis of nasopharyngeal carcinoma (NPC). Here we report that SPLUNC1 plays a role at a very early stage of NPC carcinogenesis. SPLUNC1 regulates NPC cell proliferation, differentiation and apoptosis through miR-141, which in turn regulates PTEN and p27 expression. This signaling axis is negatively regulated by the EBV-coded gene LMP1. Therefore we propose that SPLUNC1 suppresses NPC tumor formation and its inhibition by LMP1 provides a route for NPC tumorigenesis.
    PLoS ONE 01/2013; 8(3):e56929. · 3.73 Impact Factor
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    ABSTRACT: Chemoresistance is a major obstacle in cancer treatment. Our previous studies have shown that miR-125b plays an important role in chemoresistance. Here we report a novel mechanism that upregulation of miR-125b through Wnt signaling by Snail enriches cancer stem cells. Overexpression of Snail dramatically increases the expression of miR-125b, through Snail activated Wnt/beta-catenin/TCF4 axis. Snail confers chemoresistance by repressing Bak1 through upregulation of miR-125b. Restoring the expression of Bak1 or depleting miR-125b re-sensitizes Snail-expressing cancer cells to Taxol, indicating that miR-125b is critical in Snail-induced chemoresistance. Moreover, overexpression of miR-125b significantly increases the cancer stem cell population (CD24-CD44+), while depletion of miR-125b or rescue of the expression of Bak1 increases the non-stem cell population (CD24+CD44+) in Snail-overexpressing cells. These findings strongly support that miR-125b functions as a key mediator in Snail-induced cancer stem cells and chemoresistance. This novel mechanism for Snail-induced stem cell propagation and chemoresistance may have important implications in the development of strategies for overcoming cancer cell resistance to chemotherapy.
    Journal of Biological Chemistry 12/2012; · 4.65 Impact Factor
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    ABSTRACT: We develop a facile hydrothermal synthesis method to fabricate mesoporous Ni–Co oxides nanowire arrays on ordered TiO2 nanotubes (Ni–Co oxides NWs@TiO2NTs) as a high-capacity pseudocapacitor material. The composite electrode presented the highest specific capacitance of 2353 F g−1 at a charge and discharge current density of 2.5 A g−1 with excellent cycling ability, retaining 95% of the maximum capacitance after 3000 cycles. Even at a high current density of 50 A g−1, the electrode exhibited a specific capacitance of up to 2173 F g−1. In addition, the testing of a (Ni–Co oxides NWs@TiO2NTs)//(Ni–Co oxides NWs@TiO2NTs) symmetric cell yielded a specific capacitance of up to 144 F g−1 at a current density of 4 A g−1. The much improved capacity and cycling stability may be attributed to the superior conductivity and the aligned structure of the Ni–Co oxides NWs and the TiO2NTs substrate, which can improve electron/ion transport and enhance the kinetics of the redox reactions.
    J. Mater. Chem. A. 12/2012; 1(3):594-601.
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    Science China. Life sciences 12/2012; 55(12):1120-4. · 2.02 Impact Factor
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    ABSTRACT: Different from the classical configuration CuO/CeO2 catalyst, the inverse configuration CeO2/CuO catalyst (atomic ratio of Ce/Cu = 10/100) was prepared by impregnation method. Five calcination temperatures were selected to investigate the interaction between CeO2 and CuO support. It is found that as calcination temperature increased from 500 to 900°C, sintering of CeO2 particles on the support occurred together with the diffusion of a portion of Ce4+ ions into CuO crystals, forming solid solution. Formation of interface complex Ce-O-Cu was suggested by TPR measurements. The catalyst calcined at 700°C gives the highest activity for preferential oxidation of CO in excess H2 stream.
    Journal of Natural Gas Chemistry 09/2012; 21(5):513–518. · 1.41 Impact Factor
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    ABSTRACT: Lactoferrin (LF) is a multifunctional glycoprotein that plays an important role in native immune defense against infections, including human herpetic viruses, such as cytomegalovirus and herpes simplex virus types 1 and 2. However, its anti-Epstein-Barr virus (EBV, a γ-herpesvirus) function has not been reported in the literature. EBV is widespread in all human populations and is believed to be linked to tumorigenesis, such as lymphomas and nasopharyngeal carcinoma (NPC). We previously reported that LF expressed a significantly lower level in NPC tissues and was a likely tumor suppressor. Since EBV infection is a major carcinogen of NPC development, we investigated the effect of LF on EBV infection and found that LF could protect human primary B lymphocytes and nasopharyngeal epithelial cells from EBV infection, but had no effect on EBV genome DNA replication. LF prevented EBV infection of primary B cells mediated by its direct binding to the EBV receptor (CD21) on the B-cell surface. Tissue array immunohistochemistry revealed that LF expression was significantly downregulated in NPC specimens, in which high EBV viral capsid antigen-IgA levels were observed. These data suggest that LF may inhibit EBV infection and that its downregulation could contribute to NPC development.
    Journal of Innate Immunity 03/2012; 4(4):387-98. · 4.46 Impact Factor
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    ABSTRACT: Ni nanoparticles were loaded on TiO2 nanotube arrays (Ni/TiO2NTs) via pulsed electrodeposition method and employed as catalyst for methanol oxidation in alkaline media. The as-prepared Ni/TiO2NTs catalyst was characterized by field emission scanning electron microscopy (FESEM), X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS) and electrochemical analyzer. The electrochemical studies showed that Ni/TiO2NTs under illumination exhibited higher catalytic activity and stronger poisoning-tolerance for methanol oxidation than that in the dark. The effect of illumination which improved catalytic activity of Ni/TiO2NTs were attributed to the p–n junction formed at the interface between Ni(OH)2 and TiO2NTs resulting in the photo-generated holes flow into Ni(OH)2, thus, the transmitted holes boosted the oxidation of Ni(OH)2 and produced the OH to oxidize methanol and intermediates that absorbed on the catalyst. The present study shows Ni/TiO2NTs can act as a promising candidate for the anode catalyst in photo assist direct methanol fuel cells (PDMFCs) application.
    International Journal of Hydrogen Energy 03/2012; 37(6):4967–4973. · 3.55 Impact Factor

Publication Stats

833 Citations
171.49 Total Impact Points


  • 2014
    • The Third Xiangya Hospital of the Central South University
      Ch’ang-sha-shih, Hunan, China
  • 2011–2014
    • Chongqing University
      • Department of Chemical Engineering
      Ch’ung-ch’ing-shih, Chongqing Shi, China
  • 2002–2014
    • Central South University
      • Cancer Research Institute
      Ch’ang-sha-shih, Hunan, China
  • 2011–2012
    • Beijing Institute Of Technology
      • School of Chemistry
      Peping, Beijing, China
  • 2010–2012
    • University of South Alabama
      • Department of Cell Biology and Neuroscience
      Mobile, Alabama, United States
  • 2002–2004
    • Xiangya Hospital of Central South University
      Ch’ang-sha-shih, Hunan, China
  • 1999–2001
    • Changsha Medical University
      Ch’ang-sha-shih, Hunan, China