Ming Wang

Shanghai Jiao Tong University, Shanghai, Shanghai Shi, China

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Publications (8)30.5 Total impact

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    ABSTRACT: The impact of cellular oxidative stress in promoting the epithelial-mesenchymal transition (EMT) has been noticed. Our previous study shows that SENP3, a redox-sensitive SUMO2/3-specific protease, accumulates in a variety of cancers, but whether SENP3 and SUMOylation involve in the regulation of EMT is unclear. The present study uncovers a novel role of SENP3 in promoting the EMT process in gastric cancer via regulating an EMT-inducing transcription factor, forkhead box C2 (FOXC2). We demonstrate that the expression of mesenchymal marker genes and cell migration ability are enhanced in SENP3-overexpressing gastric cancer cells and attenuated in SENP3-knockdown cells. A nude mouse model and a set of patient's specimens suggest the correlation between SENP3 and gastric cancer metastasis. Biochemical assays identify FOXC2 as a substrate of SENP3. Meanwhile N-cadherin is verified as a target gene of FOXC2, which is transcriptionally activated by a SUMO-less FOXC2. Additionally, reactive oxygen species-induced de-SUMOylation of FOXC2 can be blocked by silencing endogenous SENP3. In conclusion, SENP3, which is increased in gastric cancer cells, potentiates the transcriptional activity of FOXC2 through de-SUMOylation, in favor of the induction of specific mesenchymal gene expression in gastric cancer metastasis.
    Oncotarget 08/2014; 5(16):7093-7104. · 6.63 Impact Factor
  • Qin Chen, Tao Zhao, Ming Wang, Jing Wang
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    ABSTRACT: Calotropis gigantea, kapok and cotton fibres are all natural cellulose fibres, but the first of these is rarely used in textile fabrics. In this study, the structure and chemical composition of these three kinds of fibre were studied, and the dyeing properties of fabrics made from each of them were compared. The purpose of this was to provide a theory basis for the application of C. gigantea fibre in the textile industry. The surface morphology and cross-section of C. gigantea fibre in comparison with kapok and cotton were studied by scanning electron microscopy. Their fibrous structures were analysed by Fourier Transform-infrared spectroscopy and X-ray diffraction. The mechanical properties and water absorption capabilities were also measured and compared. Both C. gigantea fibre and kapok fibre exhibit a high degree of hollowness (80–90%), and no natural twist exists; there is a certain amount of lignin and hemicellulose in C. gigantea fibres; the crystallinity of C. gigantea fibres is 42.54%, and its crystallinity orientation index is 85.40%. C. gigantea fibre has the lowest tenacity but has the highest water content of the three kinds of fibre. The results of dyeing tests show that C. gigantea fabric has the lowest dye uptake and dye fixation.
    Coloration Technology 12/2013; 129(6). DOI:10.1111/cote.12051 · 1.17 Impact Factor
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    ABSTRACT: Emerging studies have indicated that microRNAs are involved in the development and progression of cancer. Here we found that miR-202-3p was frequently down-regulated in gastric cancer tissues. Overexpression of miR-202-3p in gastric cancer cells MKN-28 and BGC-823, markedly suppressed cell proliferation and induced cell apoptosis both in vitro and in vivo. Furthermore, Gli1 expression was frequently positive in gastric cancer tissues and inversely correlated with miR-133b expression. We demonstrate that the transcriptional factor Gli1 was a target of miR-202-3p and plays an essential role as a mediator of the biological effects of miR-202-3p in gastric cancer. MiR-202-3p also inhibited the expression of γ-catenin and BCL-2. Taken together, these findings suggest that miR-202-3p may function as a novel tumor suppressor in gastric cancer and its anti-tumor activity may attribute the direct targeting and inhibition of Gli1.
    PLoS ONE 07/2013; 8(7):e69756. DOI:10.1371/journal.pone.0069756 · 3.53 Impact Factor
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    ABSTRACT: BACKGROUND: MicroRNAs can promote or suppress the evolution of malignant behaviors by regulating multiple targets. We aimed to determine the expression of miR-301a recently screened in gastric cancer, to investigate the biological effects of miR-301a and to identify the specific miR-301a target gene. METHODS: Quantitative real-time RT-PCR was used to test miR-301a expression. Functional effects were explored by a water-soluble tetrazolium salt assay, a colony formation assay in soft agar, a migration assay, an invasion assay and cytometry used to determine apoptosis and cell cycle. Nude mice were inoculated subcutaneously by retrovirus-mediated stably expressed SGC-7901 cells. The target gene was determined by bioinformatic algorithms, dual luciferase reporter assay and Western blot. RESULTS: Firstly, we found that miR-301a was significantly upregulated both in cells and tissues of gastric cancer. The expression level of miR-301a was inversely correlated with tumor differentiation of gastric cancer tissues. Secondly, miR-301a promoted cell growth, soft agar clonogenicity, migration, invasion, and decreased cell apoptosis induced by cisplatin in vitro, while blockage of miR-301a reduced the percentage of G2/M phase cells via flow cytometry in gastric cancer cells. Ectopic expression of miR-301a enhanced the subcutaneous tumorigenesis in vivo. Finally, miR-301a directly downregulated RUNX3 expression post-transcriptionally in gastric cancer. CONCLUSION: Our results demonstrate that miR-301a plays important roles in the development of gastric cancer.
    Journal of Gastroenterology 01/2013; DOI:10.1007/s00535-012-0733-6 · 4.02 Impact Factor
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    ABSTRACT: Accumulating evidence has shown that microRNAs are involved in multiple processes in cancer development and progression. Here, we report that expression of miR-625 is significantly down-regulated and negatively correlated with lymph node metastasis in gastric cancer. miR-625 significantly inhibits invasion and metastasis of gastric cancer cells both in vitro and in vivo. Moreover, we identify that ILK is a direct target gene for miR-625 and knockdown of ILK has a phenocopy of overexpression of miR-625. Taken together, our findings suggest that miR-625 plays an important role in the mechanism of tumor metastasis.
    FEBS letters 06/2012; 586(16):2382-8. DOI:10.1016/j.febslet.2012.05.050 · 3.34 Impact Factor
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    ABSTRACT: microRNA-155 (miR-155), an important multifunctional microRNA, has been implicated in the development of multiple solid tumors, yet, its role in gastric cancer cells has not been fully elucidated. In this study, we find that miR-155 was significantly downregulated in gastric cancer cell lines compared with an immortalized gastric epithelial cell line (GES-1). Overexpression of miR-155 in SGC-7901 and MKN-45 gastric cancer cells dramatically suppressed cell migration, invasion and adhesion in vitro. Overexpression of miR-155 significantly reduced the protein levels of SMAD2 and repressed the activity of a luciferase reporter containing one of the two predicted miR-155 binding sites in SMAD2 3'-UTR, indicating that SMAD2 may be a miR-155 target gene. miR-155 expression was also remarkably restored by a DNA demethylating agent (5-Aza-2-deoxycytidine) in SGC-7901 and MKN-45 gastric cancer cells. Taken together, these data suggest that miR-155 may function as a tumor suppressor to regulate gastric cancer cell metastasis by targeting SMAD2, and its downregulation in gastric cancer cells may be partly ascribed to DNA methylation.
    Oncology Reports 03/2012; 27(6):1960-6. DOI:10.3892/or.2012.1719 · 2.19 Impact Factor
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    ABSTRACT: Emerging evidence has indicated microRNAs are involved in tumor development and progression, acting as tumor suppressors or oncogenes. Here we report that miR-409-3p was significantly downregulated in gastric cancer (GC) cell lines and tissues. Overexpression of miR-409-3p in SGC-7901 gastric cancer cells dramatically suppressed cell proliferation and induced cell apoptosis both in vitro and in vivo. Furthermore, we demonstrate that the transcriptional regulator PHF10 was a target of miR-409-3p. Taken together, these findings suggest that miR-409-3p may function as a novel tumor suppressor in GC and its anti-oncogenic activity may involve the direct targeting and inhibition of PHF10.
    Cancer letters 02/2012; 320(2):189-97. DOI:10.1016/j.canlet.2012.02.030 · 5.02 Impact Factor
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    ABSTRACT: Small ubiquitin-like modifier (SUMO) 2/3 is known to conjugate to substrates in response to a variety of cellular stresses. However, whether and how SUMO2/3-specific proteases are involved in de-conjugation under cell stress is unclear. Here, we show that low doses of hydrogen peroxide (H(2)O(2)) induce an increase of the SENP3 protein, which removes SUMO2/3 from promyelocytic leukemia (PML). Low dose H(2)O(2) causes SENP3 to co-localize with PML bodies and reduces the number of PML bodies in a SENP3-dependent manner. Furthermore, de-conjugation of SUMO2/3 from PML is responsible for the accelerated cell proliferation caused by low dose H(2)O(2). Knocking down PML promotes basal cell proliferation as expected. This can be reversed by reconstitution with wild-type PML but not its mutant lacking SUMOylation, indicating that only the SUMOylated PML can play an inhibitory role for cell proliferation. Thus, SENP3 appears to be a key mediator in mild oxidative stress-induced cell proliferation via regulation of the SUMOylation status of PML. Furthermore, SENP3 is over-accumulated in a variety of primary human cancers including colon adenocarcinoma in which PML is hypo-SUMOylated. These results reveal an important role of SENP3 and the SUMOylation status of PML in the regulation of cell proliferation under oxidative stress.
    Journal of Biological Chemistry 02/2010; 285(17):12906-15. DOI:10.1074/jbc.M109.071431 · 4.60 Impact Factor

Publication Stats

108 Citations
30.50 Total Impact Points


  • 2012–2014
    • Shanghai Jiao Tong University
      • School of Medicine
      Shanghai, Shanghai Shi, China
    • Ruijin Hospital North
      Shanghai, Shanghai Shi, China
  • 2013
    • Donghua University
      • College of Chemistry, Chemical Engineering & Biotechnology
      Shanghai, Shanghai Shi, China