Jin Wang

Peking University, Peping, Beijing, China

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Publications (10)17.14 Total impact

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    ABSTRACT: Hypoxia-inducible factor-1 (HIF-1) is a major determinant of invasion and metastasis in several tumor types. We previously reported that HIF-1α contributed to multidrug resistance in gastric cancer. However, the role of HIF-2α on the progression of gastric cancer is seldom reported. In this study, we first examined the possible role of HIF-1α and HIF-2α in the process of invasiveness and metastasis of gastric cancer, using immunohistochemistry of 80 gastric cancer tissues, western blot and real-time PCR of 8 fresh gastric cancer tissues. The results showed that HIF-1α and HIF-2α were significantly correlated with the clinical stage and were highly expressed in metastatic gastric cancers compared to nonmetastatic ones. Western blot analysis revealed that hypoxia (1% O₂, 8 h) induced HIF-1α and HIF-2α expression in different gastric cancer cell lines, including SGC7901, AGS, MGC803 and MKN45. Adhesion and invasion assays found that hypoxia caused an increase in adhesive and invasive abilities of gastric cancer cells. Small interfering (si) RNA against HIF-1α and HIF-2α in SGC7901 cells significantly inhibited hypoxia-induced adhesive and invasive abilities. Finally, the JNK inhibitor SP 600125 abolished hypoxia-induced HIF-1α and HIF-2α expression, and inhibited the adhesive and invasive abilities of gastric cancer cells exposed to hypoxia in a dose-dependent manner. Taken together, the present work suggested that HIF-1α and HIF-2α were involved in metastasis and invasion of gastric cancer cells under hypoxia, with the involvement of JNK signal pathway.
    Cancer biology & therapy 08/2010; 10(4):376-82. · 3.29 Impact Factor
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    ABSTRACT: To describe the phenotypic changes of Schwann cells during nerve regeneration, we made two different neurorrhaphy models after rat sciatic nerves injury, the epineurium neurorrhaphy and small gap bridging suture. Then, at selected time points after surgery (1d, 3d, 5d, 7d, 2 weeks, 3 weeks), the materials were drawn for detecting the expression of GFAP, Sox2, Krox20 by immunofluorescence. GFAP is expressed in non-myelin-forming Schwann cells and Krox20 is a marker for myelin-forming cells in the adult nerve. Sox2 is a marker for neural stem and progenitor cells. Our findings showed the rule of phenotypic changes of Schwann cells during nerve regeneration. Furthermore, the difference in the phenotypic changes of Schwann cells between two operation methods indicated that the small gap changes the regenerated microenvironment and may be one of the reasons that small gap bridging suture is superior to the epineurium suture.
    Artificial Cells Blood Substitutes and Biotechnology (formerly known as Artificial Cells Blood Substitutes and Immobilization Bi 01/2010; 38(1):24-8. · 0.94 Impact Factor
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    ABSTRACT: To determine whether insulin administration modulates the systemic inflammatory response in infants undergoing cardiac surgery with cardiopulmonary bypass, 60 infants undergoing cardiopulmonary bypass were randomly assigned into a routine therapy group or to an intensive insulin therapy group with 30 infants in each group. Plasma IL-1beta, IL-6, IL-10, and TNF-alpha levels were determined before anesthesia, at the initiation of cardiopulmonary bypass, and at 0, 6, 12, 24, and 48 h after cardiopulmonary bypass. Nuclear factor-kappaBp65 expression and IkappaB expression in peripheral blood mononuclear cells were also measured by Western blot analysis. TNF-alpha, IL-1beta, IL-6, and IL-10 levels were all elevated after the initiation of cardiopulmonary bypass. However, TNF-alpha, IL-1beta, and IL-6 levels were significantly attenuated in the intensive insulin therapy group compared to those in the routine therapy group after initiation of cardiopulmonary bypass (p<0.05 or <0.01). Meanwhile, plasma IL-10 levels were significantly higher in the intensive insulin therapy group than in the routine therapy group after initiation of cardiopulmonary bypass (p<0.05 or <0.01). Accordingly, Nuclear factor-kappaBp65 expression and IkappaB expression were significantly increased after initiation of cardiopulmonary bypass in both groups (p<0.05 or <0.01). The expression of Nuclear factor-kappaBp65, which induces the transcription of pro-inflammatory cytokines was significantly attenuated in the intensive insulin therapy group (p<0.05 or <0.01). Meanwhile, the expression of IkappaB, an inhibitor of NF-kappaB, was significantly higher in the intensive insulin therapy group (p<0.05 or <0.01). These results suggested that intensive insulin therapy may attenuate the systemic inflammatory response in infants undergoing cardiopulmonary bypass.
    Cytokine 10/2008; 44(1):96-100. · 2.52 Impact Factor
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    ABSTRACT: We have investigated the roles of dopamine and cAMP-regulated phosphoprotein (DARPP-32) in the multidrug resistance (MDR) of gastric cancer cells and the possible underlying mechanisms. The up-regulation of DARPP-32 was found to significantly enhance the sensitivity of cells of human adriamycin (ADR)-resistant gastric adenocarcinoma cell line SGC7901/ADR to vincristine, ADR, 5-fludrouracil and cisplatin. The results of an in vivo drug sensitivity assay confirmed that DARPP-32 may play a specific role in the MDR of gastric cancer. DARPP-32 significantly down-regulated the expression of P-glycoprotein and zinc ribbon domain-containing 1 (ZNRD1), but did not alter the expression of MDR-associated protein or glutathione-S-transferase. The up-regulation of ZNRD1 significantly inhibited the drug sensitivity of gastric cancer cells over-expressing DARPP-32, indicating that ZNRD1 may be important in the DARPP-32-mediated MDR of gastric cancer. DARPP-32 was also able to significantly decrease the anti-apoptotic activity of SGC7901/ADR cells. Further study of the biological functions of DARPP-32 may be helpful for understanding the mechanisms of MDR of gastric cancer cells and developing possible strategies to treat gastric cancer.
    Digestive Diseases and Sciences 02/2008; 53(1):101-7. · 2.26 Impact Factor
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    ABSTRACT: Here, we firstly investigated the roles of DARPP-32 in multidrug resistance of gastric cancer cells. Inhibition of DARPP-32 by small interfering RNA led to decreased sensitivity of cells to chemotherapeutic drugs, accompanied by increased capacity of cells to efflux adriamycin. Inhibition of DARPP-32 expression could significantly up-regulate the expression of permeability glycoprotein (P-gp) and zinc ribbon domain-containing 1 (ZNRD1), but not alter the expression of multidrug resistance-associated protein or glutathione transferase. The DARPP-32 siRNA-mediated MDR could be reversed by inhibitor of P-gp or siRNA of ZNRD1, indicating DARPP-32 might mediate MDR of gastric cancer through regulation of P-gp and ZNRD1.
    Cancer Investigation 01/2008; 25(8):699-705. · 2.24 Impact Factor
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    ABSTRACT: Here we investigated the roles of DARPP-32 in multidrug resistance (MDR) of gastric cancer cells and the possible underlying mechanisms. We constructed the eukaryotic expression vector of DARPP-32 and transfected it into human vincristine-resistant gastric adenocarcinoma cell line SGC7901/VCR. Up-regulation of DARPP-32 could significantly enhance the sensitivity of SGC7901/VCR cells towards vincristine, adriamycin, 5-fluorouracil and cisplatin, and could decrease the capacity of cells to efflux adriamycin. What's more, the results of subrenal capsule assay confirmed that DARPP-32 might play a certain role in MDR of gastric cancer. DARPP-32 could significantly down-regulate the expression of P-gp and zinc ribbon domain-containing 1 (ZNRD1), but not alter the expression of multidrug resistance-associated protein (MRP) or the glutathione S-transferase (GST). DARPP-32 could also significantly decrease the anti-apoptotic activity of SGC7901/VCR cells. Further study of the biological functions of DARPP-32 might be helpful for understanding the mechanisms of MDR in gastric cancer.
    Cell Biology International 10/2007; 31(9):1010-5. · 1.64 Impact Factor
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    ABSTRACT: The Id family of helix-loop-helix proteins is involved in a variety of biological processes, including development,proliferation, and angiogenesis. There is emerging evidence for deregulation of Id proteins in some cancers. Hence we determined Id expression in gastric cancer. To elucidate the involvement of Idl in gastric carcinogenesis, Immunohistochemistry was carried out on paraffin-embedded gastric cancer sections. By analyzing the relationship between the Idl staining index of individual tumors and the patient's clinical parameters, including histological grade, clinical stage, and presence of metastases, we found that strong Idl expression was associated with poorer differentiation and more aggressive behavior of tumor cells. To further explore Idl expression in human gastric carcinomas, Western blot analysis was performed to analyze Idl protein expression in 15 pairs of gastric tissues and cancers and in gastric cell lines. Idl was found to be expressed at higher levels in 11/15 cancer tissues compared to adjacent tissues. Idl was upregulated more prominently in the poorly differentiated cell lines than in the well-differentiated ones. Semiquantitative RT-PCR was carried out to investigate the expression of mRNA of Idl in gastric cancer cell lines and it was upregulated in most of them. Our results demonstrate that Idl protein may play an important role in the process of gastric carcinogenesis and high-level Id I expression may be related to the malignant potential of tumor cells.
    Cancer Letters 01/2005; 216(1):63-71. · 4.26 Impact Factor
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    ABSTRACT: To investigate the significance of DARPP-32 protein expression in gastric carcinoma tissue and cell lines. The expression of DARPP-32 protein in normal gastric mucosa and gastric carcinoma tissue was evaluated by immunohistochemical staining using streptavidin-biotin complex technique. The expression in gastric carcinoma tissue and cell lines was evaluated by Western blotting. The expression rate of DARPP-32 protein in gastric adenocarcinoma tissue (92.7%) was significantly higher than that in normal gastric mucosa (52.6%, P < 0.05). There was no significant association between DARPP-32 protein expression and degree of tumor differentiation, local invasion and distant metastasis. As compared with adjacent non-carcinomatous gastric mucosa, both DARPP-32 and its truncated isoform t-DARPP were overexpressed in gastric adenocarcinoma tissue (t = 2.45, P = 0.015); and t-DARPP overexpression was more frequently seen. Expression of DARPP-32 and t-DARPP could also be detected in human gastric cancer cell lines. The expression of DARPP-32 protein was obviously reduced in SGC7901 drug-resistant cell strains. DARPP-32 is overexpressed in gastric carcinoma. It may play an important role in gastric carcinogenesis. The underlying signal pathways in neoplastic gastric epithelium may also be related to the multi-drug resistance property of gastric cancer cells.
    Zhonghua bing li xue za zhi Chinese journal of pathology 08/2004; 33(4):350-3.
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    ABSTRACT: We have efficiently generated the first monoclonal antibody (MAb) against the human ZNRD1 protein, a transcription-associated protein, consisting of two zinc ribbon domains. Hybridomas were screened by indirect enzyme-linked immunosorbent assay (ELISA) using either purified 6 x His-ZNRD1fusion protein or purified 6 x His-OS-9 fusion protein as a control. One MAb named H6 (IgG(1)), effective in detecting the recombinant and cellular protein, was characterized by ELISA and Western immunoblotting. Thus, it binds to native ZNRD1 protein and should be useful in studies of ZNRD1 protein function and expression. By Western immunoblotting analysis of 16 patients with gastric cancer using the MAb, we found ZNRD1 protein was more overexpressed in incision margin than in carcinoma tissue. The results showed that ZNRD1 might be a novel modifier in gastric carcinogenesis.
    Hybridoma and Hybridomics 03/2004; 23(1):65-8.
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    ABSTRACT: The Id family of helix–loop–helix proteins is involved in a variety of biological processes, including development, proliferation, and angiogenesis. There is emerging evidence for deregulation of Id proteins in some cancers. Hence we determined Id expression in gastric cancer. To elucidate the involvement of Id1 in gastric carcinogenesis, Immunohistochemistry was carried out on paraffin-embedded gastric cancer sections. By analyzing the relationship between the Id1 staining index of individual tumors and the patient's clinical parameters, including histological grade, clinical stage, and presence of metastases, we found that strong Id1 expression was associated with poorer differentiation and more aggressive behavior of tumor cells. To further explore Id1 expression in human gastric carcinomas, Western blot analysis was performed to analyze Id1 protein expression in 15 pairs of gastric tissues and cancers and in gastric cell lines. Id1 was found to be expressed at higher levels in 11/15 cancer tissues compared to adjacent tissues. Id1 was upregulated more prominently in the poorly differentiated cell lines than in the well-differentiated ones. Semiquantitative RT-PCR was carried out to investigate the expression of mRNA of Id1 in gastric cancer cell lines and it was upregulated in most of them. Our results demonstrate that Id1 protein may play an important role in the process of gastric carcinogenesis and high-level Id1 expression may be related to the malignant potential of tumor cells.
    Cancer Letters - CANCER LETT. 01/2004; 216(1):63-71.