Browsing by Author "Li, Chi-Han"

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A potential role for Helicobacter pylori heat shock protein 60 in gastric tumorigenesis
(2010-02-05)
Lin, Chen-Si
;
He, Pei-Juin
;
Tsai, Nu-Man
;
Li, Chi-Han
;
Yang, Shang-Chih
Helicobacter pylon has been found to promote the malignant process leading to gastric cancer. Heat shock protein 60 of H. pylori (HpHSP60) was previously been identified as a potent immunogene. This Study investigates the role of HpHSP60 in gastric cancer carcinogenesis. The effect of HpHSP60 on cell proliferation, anti-death activity, angiogenesis and cell migration were explored. The results showed that HpHSP60 enhanced migration by gastric cancer cells and promoted tube formation by umbilical vein endothelial cells (HUVECs); however, HpHSP60 did not increase cell Proliferation nor was this protein able to rescue gastric cancer cells from death. Moreover, the results also indicated HpHSP60 had different effects on AGS gastric cancer cells or THP-1 monocytic cells in terms of their expression of pro-inflammatory cytokines, which are known to be important to cancer development. We propose that HpHSP60 may trigger the initiation of carcinogenesis by inducing pro-inflammatory cytokine release and by promoting angiogenesis and metastasis. Thus, this extracellular pathogen-derived HSP60 is potentially a vigorous virulence factor that can act as a carcinogen during gastric tumorigenesis. (C) 2010 Elsevier Inc. All rights reserved.
Characterizing the polymeric status of Helicobacter pylori heat shock protein 60
(2009-10-16)
Lin, Ching-Yi
;
Huang, Yu-Shan
;
Li, Chi-Han
;
Hsieh, Yuan-Ting
;
Tsai, Nu-Man
Helicobacter pylori heat shock protein 60 (HpHsp60) was first identified as an adhesion molecule associated with H. pylori infection. Here we have analyzed the structure of HpHsp60 via amino acid BLAST, circular dichroism, and electrophoresis and the results indicate that most recombinant HpHsp60 molecules exist as dimers or tetramers, which is quite different from Escherichia coli Hsp60. Treatment of human monocytic cells THP-1 with HpHsp60 was found to up-regulate a panel of cytokines including IL-1 alpha, IL-8, IL-10, IFN-gamma, TNF-alpha, TGF-beta, GRO, and RANTES. Carboxymethylated HpHsp60 molecules with a switched oligomeric status were able to further enhance NF-kappa B-mediated IL-8 and TNF-alpha secretion in THP-1 cells compared to unmodified HpHsp60 molecules. These results indicated that the oligomeric status of HpHsp60s might have an important role in regulating host inflammation and thus help facilitate H. pylori persistent infection. (C) 2009 Elsevier Inc. All rights reserved.
Enhancement of anti-murine colon cancer immunity by fusion of a SARS fragment to a low-immunogenic carcinoembryonic antigen
(1970-01-01)
Lin, Chen-Si
;
Kao, Shih-Han
;
Chen, Yu-Cheng
;
Li, Chi-Han
;
Hsieh, Yuan-Ting
"Background: It is widely understood that tumor cells express tumor-associated antigens (TAAs), of which many are usually in low immunogenicity; for example, carcinoembryonic antigen (CEA) is specifically expressed on human colon cancer cells and is viewed as a low-immunogenic TAA. How to activate host immunity against specific TAAs and to suppress tumor growth therefore becomes important in cancer therapy development. Results: To enhance the immune efficiency of CEA in mice that received, we fused a partial CEA gene with exogenous SARS-CoV fragments. Oral vaccination of an attenuated Salmonella typhimurium strain transformed with plasmids encoding CEA-SARS-CoV fusion gene into BALB/c mice elicited significant increases in TNF-alpha and IL-10 in the serum. In addition, a smaller tumor volume was observed in CT26/CEA-bearing mice who received CEA-SARS-CoV gene therapy in comparison with those administered CEA alone. Conclusion: The administration of fusing CEA-SARS-CoV fragments may provide a promising strategy for strengthening the anti-tumor efficacy against low-immunogenic endogenous tumor antigens."
The treatment of propofol induced the TGF-beta 1 expression in human endothelial cells to suppress endocytosis activities of monocytes
(2010-12-01)
Li, Chi-Han
;
Lee, Ru-Ping
;
Lin, Yu-Ling
;
Lin, Chen-Si
;
Hsu, Bang-Gee
Propofol anesthesia and sedation are known to downregulate the functions of many hematopoietic cells, such as macrophages and neutrophils, in vivo. However, the effects of propofol on secretion of the regulatory cytokine transforming growth factor beta 1 (TGF-beta 1) in vivo are unknown. In this study, the effects of propofol on TGF-beta 1 expression in human peripheral blood mononuclear cells, umbilical vein endothelial cells (HUVECs), lymphocytes (Jurkat) and monocytes (THP-1) were tested. Moreover, these sera were also tested for regulatory activity on monocyte endocytosis with or without treatment with the TGF-beta 1 pathway inhibitor SB431542. Propofol raised levels of both total and activated TGF-beta 1 in propofol-treated patient sera after surgical operations. Furthermore, propofol induced secretion of latent TGF-beta 1 in HUVEC cells and enhanced TGF-beta 1 activation in THP-1 and Jurkat cells in vitro. Additionally, sera from propofol-treated patients suppressed monocyte endocytosis ex vivo, an effect that was abrogated by the TGF-beta 1 pathway inhibitor SB431542. (C) 2010 Elsevier Ltd. All rights reserved.