Xiangmin Tong
Zhejiang University
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Featured researches published by Xiangmin Tong.
Acta Biochimica et Biophysica Sinica | 2015
Shuangshuang Li; Xiangli Gao; Xiaoxin Wu; Zhigang Wu; Linfang Cheng; Lifen Zhu; Dan Shen; Xiangmin Tong
Parthenolide (PTL) shows potent anti-inflammatory and anti-cancer activities. In the present study, the molecular mechanisms of PTLs activities were explored in lipopolysaccharide (LPS)-induced human leukemia monocytic THP-1 cells and human primary monocytes. The 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium salt (MTS) assay was used to analyze the effect of PTL on THP-1 cell viability. Enzyme-linked immunosorbent assay was used to determine the effect of PTL on LPS-induced inflammatory cytokine secretion. Flow cytometry and quantitative real-time polymerase chain reaction were used to assess the effect of PTL on LPS-induced toll-like receptor 4 (TLR4) expression. Phosphorylation levels of signaling molecules were determined by western blot analysis. Results showed that PTL <12.5 μM did not significantly affect THP-1 cells viability. LPS treatment led to a marked up-regulation of interleukin (IL)-6, IL-1β, IL-8, IL-12p40, tumor necrosis factor-α, IL-18, and NO in THP-1 cells. However, PTL inhibited the expression of these cytokines in a dose-dependent manner, with IC50 values of 1.091-2.620 μM. PTL blocked TLR4 expression with an IC50 value of 1.373 μM as determined by the flow cytometry analysis, and this blocking effect was verified at both protein and mRNA levels. Up-regulation of phosphorylation levels of extracellular signal-regulated kinase 1/2, Jun N-terminal kinase, p38, nuclear factor κB (NF-κB) p65, and IκBα and up-regulation of expressions of other molecules (inducible nitric oxide synthase, TLR4, and TNF receptor-associated factor 6) induced by LPS were abolished by PTL in a dose-dependent manner. The anti-inflammatory mechanisms of PTL operate partly through the TLR4-mediated mitogen-activated protein kinase and NF-κB signaling pathways. Therefore, TLR4 may be a new target for anti-inflammation therapies.
International Journal of Laboratory Hematology | 2008
Xiangmin Tong; Hangping Yao; Wenbin Qian; Lifen Zhu; Z. H. Fu; Z. L. Huang; Jie Jin
Successful adoptive immunotherapy for leukemia depends on the generation of T cells that can specifically react with malignant cells. Dendritic cells (DCs) are important antigen‐presenting cells in the development of antileukemia T‐cell responses. Mononuclear cells (MNC) were isolated from peripheral blood or bone marrow of patients with chronic myelogenous leukemia (CML), and acute myelogenous leukemia (AML). After incubation with granulocyte‐macrophage colony‐stimulating factor, interleukin (IL)‐4, and tumor necrosis factor‐α, MNC developed morphological characteristics of DCs in vitro, which were confirmed by phenotypic assay. Fluorescence in situ hybridization demonstrated the presence of fusion gene in the nuclei of representative CML or AML–M3 samples, indicating that the cells were leukemic in origin. IL‐12 levels were significantly higher in AML–DCs and CML–DCs prestimulated with phorbol 12‐myristate 13‐acetate than in the corresponding leukemic cells, but were lower than that of healthy donors. These cells were potent stimulators of lymphocyte proliferation in specific in vitro assays for DC function. However, the stimulatory abilities of allogeneic T cells in a mixed lymphocyte reaction were impaired compared with those of mature DCs derived from healthy donors, although T‐cell stimulatory effects were significantly increased in these differentiated leukemia–DCs. These results suggest that functional DCs may be derived from leukemic (AML, CML) blasts in a significant number of patients and may be capable of inducing leukemia‐specific immune responses with potentially clinically beneficial effects.
Cancer Biology & Therapy | 2013
Xiangmin Tong; X.Y. Zhang; Jian Fan; Yin Tong; Shuangshuang Li; Jie Jin; Hangping Yao
Background: Aberrant expression of the RON receptor tyrosine kinase is associated with tumor progression and carcinogenesis. The aims of this study were to determine the role and functional mechanisms of RON in Burkitt lymphoma (BL) and to document its potential as a therapeutic target. Methods: RON expression was determined in BL cell lines by western blot analysis and examined in human lymphoma specimens by both western blotting and immunohistochemistry. The correlation between RON expression and Epstein-Barr virus (EBV) infection was investigated. Raji cells were treated with the Zt/f2 anti-RON mAb and cell viability, colony formation, apoptosis and cell cycle arrest were measured in vitro using cell proliferation assays, colony-forming assays and flow cytometry. Downregulation of RON by Zt/f2 was validated in mice bearing Raji cell xenografts. Results: Immunohistostaining showed a high frequency of RON+ cells in BL tissues and RON expression strongly correlated with EBV positivity. RON downregulation significantly decreased cell proliferation and colony formation via promotion of apoptosis and cell cycle arrest in Raji cells. The in vivo study showed that RON knockdown inhibits the tumorigenic potential of Raji cells in nude mice. Conclusions: RON acts as an oncogene in the carcinogenesis and progression of BL and is therefore a potential target for therapeutic intervention.
Acta Biochimica et Biophysica Sinica | 2007
Xiangmin Tong; Shui’er Zheng; Jie Jin; Lifen Zhu; Yinjun Lou; Hangping Yao
Annals of Hematology | 2012
Qitian Mu; Qiuling Ma; Yungui Wang; Zhimei Chen; Xiangmin Tong; Feifei Chen; Ying Lu; Jie Jin
Tropical Journal of Pharmaceutical Research | 2015
Bing-Mu Fang; Jin-Hong Jiang; X.Y. Zhang; Jian Fan; Shuangshuang Li; Xiangmin Tong
Archive | 2007
Xiangmin Tong; Jie Jin; Hangping Yao
Chinese journal of internal medicine | 2004
Xiangmin Tong; Jin J; Xue Yq; Wang Yg
Archive | 2011
Xiangmin Tong; Hangping Yao; Jie Jin
Archive | 2011
Dan Shen; Xiangmin Tong; Junyu Zhang; Panhan Zhang; Jie Jin; Xiangli Gao; Chengjian Ma