Xing-Jiang Xie

Publications of Xing-Jiang Xie

• Liposomal honokiol inhibits VEGF-D-induced lymphangiogenesis and metastasis in xenograft tumor model.

  Authors: Jing Wen, A-Fu Fu, Li-Juan Chen, Xing-Jiang Xie, Guang-li Yang, Xian-Cheng Chen, Yong-Sheng Wang, Jiong Li, Ping Chen, Ming-Hai Tang, Xi Ming Shao, You Lu, Xia Zhao, Yu-Quan Wei

  International journal of cancer. Journal international du cancer. 01/2009;

  Lymph nodes metastasis of tumor could be a crucial early step in the metastatic process. Induction of tumor lymphangiogenesis by vascular endothelial growth factor-D may play an important role inLymph nodes metastasis of tumor could be a crucial early step in the metastatic process. Induction of tumor lymphangiogenesis by vascular endothelial growth factor-D may play an important role in promoting tumor metastasis to regional lymph nodes and these processes can be inhibited by inactivation of the VEGFR-3 signaling pathway. Honokiol has been reported to possess potent antiangiogenesis and antitumor properties in several cell lines and xenograft tumor models. However, its role in tumor-associated lymphangiogenesis and lymphatic metastasis remains unclear. Here, we established lymph node metastasis models by injecting overexpressing VEGF-D Lewis lung carcinoma cells into C57BL/6 mice to explore the effect of honokiol on tumor-associated lymphangiogenesis and related lymph node metastasis. The underlying mechanisms were systematically investigated in vitro and in vivo. In in vivo study, liposomal honokiol significantly inhibited the tumor-associated lymphangiogenesis and metastasis in Lewis lung carcinoma model. A remarkable delay of tumor growth and prolonged life span were also observed. In in vitro study, honokiol inhibited VEGF-D-induced survival, proliferation and tube-formation of both human umbilical vein endothelial cells (HUVECs) and lymphatic vascular endothelial cells (HLECs). Western blotting analysis showed that liposomal honokiol-inhibited Akt and MAPK phosphorylation in 2 endothelial cells, and downregulated expressions of VEGFR-2 of human vascular endothelial cells and VEGFR-3 of lymphatic endothelial cells. Thus, we identified for the first time that honokiol provided therapeutic benefit not only by direct effects on tumor cells and antiangiogenesis but also by inhibiting lymphangiogenesis and metastasis via the VEGFR-3 pathway. The present findings may be of importance to investigate the molecular mechanisms underlying the spread of cancer via the lymphatics and explore the therapeutical strategy of honokiol on antilymphangiogenesis and antimetastasis. (c) 2008 Wiley-Liss, Inc.

• Synergistic anti-tumor effect of recombinant human endostatin adenovirus combined with gemcitabine.

  Authors: Yang Wu, Li Yang, Bing Hu, Ji-Yan Liu, Jing-Mei Su, Yan Luo, Zhen-Yu Ding, Ting Niu, Qiu Li, Xing-Jiang Xie, Yan-Jun Wen, Ling Tian, Bing Kan, Yong-Qiu Mao, Yu-Quan Wei

  Anti-cancer drugs. 07/2005; 16(5):551-7.

  Endostatin is an important endogenous inhibitor of neovascularization, which has been widely used in anti-angiogenesis therapy for cancer. To fully explore the potential of endostatin, we evaluatedEndostatin is an important endogenous inhibitor of neovascularization, which has been widely used in anti-angiogenesis therapy for cancer. To fully explore the potential of endostatin, we evaluated the anti-tumor efficacy of the combination of recombinant human endostatin adenovirus and low-dose gemcitabine in nude mice. We injected recombinant human endostatin adenovirus intratumorally plus a low dose of gemcitabine i.p. routinely. The combination treatment produced no side-effects, and resulted in marked suppression in tumor formation and growth of established human lung carcinoma xenografts in nude mice, with decreased microvessel density and increased apoptosis percentage. Our data support the idea of synergistic anti-tumor properties of endostatin plus low-dose chemotherapy against human lung cancer in vivo.

• Induction of apoptosis and tumor regression by vesicular stomatitis virus in the presence of gemcitabine in lung cancer.

  Authors: Qiu Li, Yu-Quan Wei, Yan-Jun Wen, Xia Zhao, Ling Tian, Li Yang, Yong-Qiu Mao, Bing Kan, Yang Wu, Zhen-Yu Ding [......] Fei Xiao, Chun-Hua Zou, Chun-Hua Fu, Xing-Jiang Xie, Tao Yi, Guang-Hong Tan, Lian Wang, Jing Chen, Jian Liu, Zhen-Nan Gao

  International journal of cancer. Journal international du cancer. 11/2004; 112(1):143-9.

  Vesicular stomatitis virus (VSV) has been shown to replicate rapidly in vitro and kill selectively a variety of tumor cell lines. The present study was designed to determine whether gemcitabineVesicular stomatitis virus (VSV) has been shown to replicate rapidly in vitro and kill selectively a variety of tumor cell lines. The present study was designed to determine whether gemcitabine potentiates the antitumor activity of VSV in vitro and in vivo. A549 human lung adenocarcinoma cells and LLC Lewis lung carcinoma cells were treated with VSV (0.1-10 plaque-forming units per cell) plus gemcitabine (20 nM to 20 microM). Mice bearing A549 or LLC were treated with VSV (5 x 10(4) to 1 x 10(8) plaque-forming units) daily for 5 days plus gemcitabine (5-125 mg/kg/day) once every 3 days for 4 times. Induction of apoptosis and effects on growth inhibition were assessed. The lung cancer cells treated with VSV plus gemcitabine displayed the apparently increased apoptotic cells compared with treatment with VSV or gemcitabine alone. The combined treatment with VSV plus gemcitabine induced the apparent antitumor activity with complete regression of the established lung cancer in both A549 and LLC lung cancer models and augmented the induction of apoptosis in lung cancer cells in vivo as well. This study suggests that the combined treatment with VSV plus gemcitabine may augment the induction of apoptosis in lung cancer cells in vitro and in vivo, and that the augmented antitumor activity in vivo may result from the increased induction of apoptosis in lung cancer cells. The present findings may be of importance to the further exploration of the potential application of this combined approach in the treatment of lung cancer.

• Immunogene therapy of tumors with a vaccine based on the ligand-binding domain of chicken homologous integrin beta3.

  Authors: Yan-Yan Lou, Yu-Quan Wei, Li Yang, Xia Zhao, Ling Tian, You Lu, Yan-Jun Wen, Fen Liu, Mei-Juan Huang, Bin Kang [......] Qu-Ming He, Xing-Jiang Xie, Yun-qiu Mao, Song Lei, Ji-Yan Liu, Fen Lou, Li-qun Zhou, Feng Peng, Yu Jiang, Bing Hu

  Immunological investigations. 03/2002; 31(1):51-69.

  The breaking of immune tolerance against angiogenesis-associated molecules should be a useful approach for cancer therapy by active immunity. We used chicken integrin beta3 as a model antigen toThe breaking of immune tolerance against angiogenesis-associated molecules should be a useful approach for cancer therapy by active immunity. We used chicken integrin beta3 as a model antigen to explore the feasibility of immunogene therapy of the tumors with a vaccine based on a single xenogeneic homologous gene, targeting the molecules associated with angiogenesis. To test this concept we constructed a plasmid DNA encoding the ligand-binding domain of chicken integrin beta3 (P-BD-C) and control vectors. We found that immunogene therapy of tumors with a vaccine based on the ligand-binding domain of chicken integrin beta3 (P-BD-C) was effective in both protective and therapeutic anti-tumor immunity in several tumor models in mice. Autoantibodies against integrin beta3 in sera of mice immunized with the ligand-binding domain of chicken integrin beta3 could be found by Western blot analysis and ELISA assay. The purified immunoglobulins were effective in the inhibition of endothelial cell proliferation in vitro, and in anti-tumor activity as well as in the inhibition of angiogenesis by adoptive transfer in vivo. The anti-tumor activity and the production of integrin beta3-specific autoantibodies (manifested by significantly elevated Ig G1 and Ig G2b) could be abrogated by the depletion of CD4+ T lymphocytes. These observations may provide a vaccine strategy for cancer therapy through the induction of the autoimmunity against the molecules associated with tumor growth in a cross-reaction with a single xenogeneic homologous gene and may be of importance in the further exploration of the applications of other xenogeneic homologous genes identified in human and other animal genome sequence projects in cancer therapy.

• Immunogene therapy of tumors with vaccine based on Xenopus homologous vascular endothelial growth factor as a model antigen

  Authors: Yu-Quan Wei, Mei-Juan Huang, Li Yang, Xia Zhao, Ling Tian, You Lu, Jing-mei Shu, Chong-jiu Lu, Ting Niu, Bin Kang [......] Qiu-Ming He, Fei Xiao, Yan-Yan Lou, Xing-Jiang Xie, Qiu Li, Yang Wu, Zhen-Yu Ding, Bin Hu, Min Hu, Wei Zhang

  Overcoming immune tolerance of the growth factors associated with tumor growth should be a useful approach to cancer therapy by active immunity. We used vascular endothelial growth factor (VEGF) as aOvercoming immune tolerance of the growth factors associated with tumor growth should be a useful approach to cancer therapy by active immunity. We used vascular endothelial growth factor (VEGF) as a model antigen to explore the feasibility of the immunogene tumor therapy with a vaccine based on a single xenogeneic homologous gene, targeting the growth factors associated with angiogenesis. To test this concept, we constructed a plasmid DNA encoding Xenopus homologous VEGF (XVEGF-p) and control vectors. We found that immunogene tumor therapy with a vaccine based on XVEGF was effective at both protective and therapeutic antitumor immunity in several tumor models in mice. VEGF-specific autoantibodies in sera of mice immunized with XVEGF-p could be found in Western blotting analysis and ELISA assay. The purified immunoglobulins were effective at the inhibition of VEGF-mediated endothelial cell proliferation in vitro, and at antitumor activity and the inhibition of angiogenesis by adoptive transfer in vivo. The elevation of VEGF in the sera of the tumor-bearing mice could be abrogated with XVEGF-p immunization. The antitumor activity and production of VEGF-specific autoantibodies, significantly elevated IgG1 and IgG2b, could be abrogated by the depletion of CD4+ T lymphocytes. The observations may provide a vaccine strategy for cancer therapy through the induction of autoimmunity against the growth factors associated with tumor growth in a cross reaction with single xenogeneic homologous gene and may be of importance in the further exploration of the applications of other xenogeneic homologous genes identified in human and other animal genome sequence projects in cancer therapy.