Ming Zhou

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

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Publications (89)206.88 Total impact

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    ABSTRACT: Ni-based bimetallic alloys have superior physiochemical characteristics compared to monometallic Ni. In this study, new type of low cost bimetallic NimCon (n+m=4) electrocatalysts with high active surface were synthesized on Ti substrate through a hydrogen evolution assisted electrodeposition method. The as-prepared NimCon were characterized by XRD, EDS and SEM. It was revealed that the composition, surface morphology as well as the crystal phase structure of the bimetallic NimCon electrocatalysts were significantly changed with the increased content of cobalt. Electrochemical measurements showed that the bimetallic NimCon catalysts, compared with the monometallic Ni, have superior catalytic activity and stability toward the methanol electrooxidation reaction (MOR). Additionally, Ni2Co2 sample presented the highest oxidation current density and the best durability. The mechanism study based on electrochemical experiments and density functional theory based calculations showed that the doping of Co in NimCon can signally improve the surface coverage of the redox species, weaken the CO adsorption, as well as adjust the CH3OH adsorption. Such understanding is of important directive significance to design efficient non-precious catalysts.
    ACS Applied Materials & Interfaces 12/2014; · 5.90 Impact Factor
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    ABSTRACT: Recent studies have revealed that long non-coding RNAs participate in all steps of cancer initiation and progression by regulating protein-coding genes at the epigenetic, transcriptional, and post-transcriptional levels. Long non-coding RNAs are in turn regulated by other genes, forming a complex regulatory network. The regulation networks between the p53 tumor suppressor and these RNAs in nasopharyngeal carcinoma remains unclear. The aims of this study were to investigate the regulatory roles of the TP53 gene in regulating long non-coding RNA expression profiles and to study the function of a TP53-regulated long non-coding RNA (LOC401317) in the nasopharyngeal carcinoma cell line HNE2. Long non-coding RNA expression profiling indicated that 133 long non-coding RNAs were upregulated in the human NPC cell line HNE2 cells following TP53 overexpression, while 1057 were downregulated. Among these aberrantly expressed long non-coding RNAs, LOC401317 was the most significantly upregulated one. Further studies indicated that LOC401317 is directly regulated by p53 and that ectopic expression of LOC401317 inhibits HNE2 cell proliferation in vitro and in vivo by inducing cell cycle arrest and apoptosis. LOC401317 inhibited cell cycle progression by increasing p21 expression and decreasing cyclin D1 and cyclin E1 expression and promoted apoptosis through the induction of poly(ADP-ribose) polymerase and caspase-3 cleavage. Collectively, these results suggest that LOC401317 is directly regulated by p53 and exerts antitumor effects in HNE2 nasopharyngeal carcinoma cells.
    PLoS ONE 11/2014; 9(11):e110674. · 3.53 Impact Factor
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    ABSTRACT: Our previous study demonstrated that the NGX6b gene acts as a suppressor in the invasion and migration of nasopharyngeal carcinoma (NPC). Recently we identified the novel isoform NGX6a which is longer than NGX6b. In this study, we firstly found that NGX6a was degraded in NPC cells and that this degradation was mediated by ezrin, a linker between membrane proteins and the cytoskeleton. Specific siRNAs against ezrin increase the protein level of NGX6a in these cells. During degradation, NGX6a is not ubiquitinated but is degraded through a proteasome-dependent pathway. The distribution pattern of ezrin was negatively associated with NGX6a in an immunochemistry (IHC) analysis of a nasopharyngeal carcinoma tissue microarray (TMA) and fetus multiple organ tissues and western blot analysis in nasopharyngeal (NP) and NPC cell lines, suggesting that ezrin and NGX6a are associated and are involved in the progression and invasion of NPC. By mapping the interacting binding sites, the seven-trans-membrane domain of NGX6a was found to be the critical region for the degradation of NGX6a, and the amino-terminus of ezrin is required for the induction of NGX6a degradation. The knockdown of ezrin or transfection of the NGX6a mutant CO, which has an EGF-like domain and a trans-membrane 1 domain, resulted in no degradation, significantly reducing the ability of invasion and migration of NPC cells. This study provides a novel molecular mechanism for the low expression of NGX6a in NPC cells and an important molecular event in the process of invasion and metastasis of nasopharyngeal carcinoma cells.
    Journal of Biological Chemistry 11/2014; · 4.60 Impact Factor
  • Applied Surface Science 10/2014; 315:81–89. · 2.54 Impact Factor
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    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; · 3.99 Impact Factor
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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 07/2014; 9(7):e103298. · 3.53 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; · 3.93 Impact Factor
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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 03/2014; · 1.37 Impact Factor
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    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: 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 08/2013; 8(5):e62869. · 3.53 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. · 3.27 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: Highly ordered TiO2 nanotube arrays (TiO2NTs) evenly modified by Ni–Cu nanoparticles were successfully prepared by potential step method. Their morphologies, structures, and alloy composition were characterized by FESEM, XRD and EDS, respectively. The as-prepared Ni–Cu/TiO2NTs electrodes were employed for non-enzymatic glucose detection in alkaline electrolyte and showed better electro-catalytic activity compared with Ni/TiO2NTs and Cu/TiO2NTs electrodes. Factors that affected the electrocatalysis of the electrodes were examined and optimized. Consequently, a sensitive amperometric electrode of glucose was achieved under 0.6 V vs. Ag/AgCl with a high sensitivity (1590.9 μA mM−1 cm−2), low detection limit (5 μM) and wide linear range from 10 μM to 3.2 mM (R2 = 0.993). Furthermore, the oxidable species such as ascorbic acid and uric acid showed no significant interference in determination of glucose. The experiment results revealed a very good reproducibility and high stability for the proposed Ni–Cu/TiO2NTs electrodes.
    Sensors and Actuators B Chemical 05/2013; 181:501–508. · 3.84 Impact Factor
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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; · 2.84 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 03/2013; 8(3):e56929. · 3.53 Impact Factor
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    ABSTRACT: SnO2@carbon-doping TiO2 nanotube arrays (SnO2@C-TiO2NTs) were synthesized by hydrothermal method and evaluated for lithium ion insertion and photoelectrochemical activity. The composite electrode prepared for 5 h as anode materials for lithium-ion batteries exhibited much improved electrochemical performance due to the aligned pore structure and the synergistic effect of the electrode. A capacity of 142 μA h cm−2 can be obtained after 50 discharge/charge cycles at a high current density of 200 μA cm−2. Moreover, UV–vis results of the sample showed stronger absorption intensity in the range of 200–800 nm compared with bare TiO2NTs. The composite electrode displayed the maximum photocurrent density of 1.80 mA cm−2. This is attributed to the heterojunction formed at the interface between SnO2 and TiO2NTs resulting the enhance charge separation efficiency. Eletrochemical impendence spectroscopy (EIS) also shows that SnO2@C-TiO2 NTs has a noticeably lower charge-transfer resistance.
    Journal of Alloys and Compounds 03/2013; 552:392–397. · 2.73 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; · 4.60 Impact Factor

Publication Stats

1k Citations
206.88 Total Impact Points

Institutions

  • 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