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Chitosan oligosaccharides in combination with Agaricus blazei Murill extract reduces hepatoma formation in mice with severe combined immunodeficiency

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      Abstract

      Chitosan and Agaricus blazei Murill (ABM) extracts possess antitumor activities. The aim of the present study was to investigate whether chitosan, ABM extract or the two in combination were effective against tumors in tumor-bearing mice. The mice were subcutaneously injected with SK-Hep 1 cells and were then were divided into the following six groups: Group 1, control group; group 2, chitosan 5 mg/kg/day; group 3, chitosan 20 mg/kg/day; group 4, ABM (246 mg/kg/day) and chitosan (5 mg/kg/day) combined; group 5, ABM (984 mg/kg/day) and chitosan (20 mg/kg/day) combined; and group 6, ABM (984 mg/kg/day). The mice were treated with the different concentrations of chitosan, ABM or combinations of the two for 6 weeks. The levels of glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT) and vascular endothelial growth factor (VEGF), and tissue histopathological features were examined in the surviving animals. Based on the results of the investigation, the treatments performed in groups 2, 3 and 4 were identified as being capable of reducing the weights of the tumors, however, group 4, which was treated with chitosan (5 mg/kg/day) in combination with ABM (246 mg/kg/day) was able to reduce the levels of GOT and VEGF. As a result, treatment with chitosan in combination with ABM may offer potential in cancer therapy and requires further investigation.

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      Most cited references 52

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      Patterns and emerging mechanisms of the angiogenic switch during tumorigenesis.

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        Inhibition of vascular endothelial growth factor-induced angiogenesis suppresses tumour growth in vivo.

         K J Kim,  B. Li,  J Winer (1993)
        The development of new blood vessels (angiogenesis) is required for many physiological processes including embryogenesis, wound healing and corpus luteum formation. Blood vessel neoformation is also important in the pathogenesis of many disorders, particularly rapid growth and metastasis of solid tumours. There are several potential mediators of tumour angiogenesis, including basic and acidic fibroblast growth factors, tumour necrosis factor-alpha and transforming factors-alpha and -beta. But it is unclear whether any of these agents actually mediates angiogenesis and tumour growth in vivo. Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen and an angiogenesis inducer released by a variety of tumour cells and expressed in human tumours in situ. To test whether VEGF may be a tumour angiogenesis factor in vivo, we injected human rhabdomyosarcoma, glioblastoma multiforme or leiomyosarcoma cell lines into nude mice. We report here that treatment with a monoclonal antibody specific for VEGF inhibited the growth of the tumours, but had no effect on the growth rate of the tumour cells in vitro. The density of vessels was decreased in the antibody-treated tumours. These findings demonstrate that inhibition of the action of an angiogenic factor spontaneously produced by tumour cells may suppress tumour growth in vivo.
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          Signal transduction by VEGF receptors in regulation of angiogenesis and lymphangiogenesis.

          The VEGF/VPF (vascular endothelial growth factor/vascular permeability factor) ligands and receptors are crucial regulators of vasculogenesis, angiogenesis, lymphangiogenesis and vascular permeability in vertebrates. VEGF-A, the prototype VEGF ligand, binds and activates two tyrosine kinase receptors: VEGFR1 (Flt-1) and VEGFR2 (KDR/Flk-1). VEGFR1, which occurs in transmembrane and soluble forms, negatively regulates vasculogenesis and angiogenesis during early embryogenesis, but it also acts as a positive regulator of angiogenesis and inflammatory responses, playing a role in several human diseases such as rheumatoid arthritis and cancer. The soluble VEGFR1 is overexpressed in placenta in preeclampsia patients. VEGFR2 has critical functions in physiological and pathological angiogenesis through distinct signal transduction pathways regulating proliferation and migration of endothelial cells. VEGFR3, a receptor for the lymphatic growth factors VEGF-C and VEGF-D, but not for VEGF-A, regulates vascular and lymphatic endothelial cell function during embryogenesis. Loss-of-function variants of VEGFR3 have been identified in lymphedema. Formation of tumor lymphatics may be stimulated by tumor-produced VEGF-C, allowing increased spread of tumor metastases through the lymphatics. Mapping the signaling system of these important receptors may provide the knowledge necessary to suppress specific signaling pathways in major human diseases.
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            Author and article information

            Affiliations
            [1 ]Department of Medical Education and Research, Cheng Hsin General Hospital, Taipei 112, Taiwan, R.O.C.
            [2 ]Department of Pathology, National Defense Medical Center, Division of Clinical Pathology, Tri-Service General Hospital, Taipei 112, Taiwan, R.O.C.
            [3 ]Departments of Clinical Pathology, Cheng Hsin General Hospital, Taipei 112, Taiwan, R.O.C.
            [4 ]Departments of Anatomical Pathology, Cheng Hsin General Hospital, Taipei 112, Taiwan, R.O.C.
            [5 ]Division of Gastroenterology, Cheng Hsin General Hospital, Taipei 112, Taiwan, R.O.C.
            [6 ]Department of Medical Laboratory Science and Biotechnology, Yuanpei University, Hsinchu 300, Taiwan, R.O.C.
            [7 ]Department of Medical Technology, Jen-Teh Junior College of Medicine, Nursing and Management, Miaoli 356, Taiwan, R.O.C.
            [8 ]Department of Biology, Ching Cheng High School, Changhua 500, Taiwan, R.O.C.
            [9 ]School of Chinese Medicine for Post Baccalaureate, I Shou University, Kaohsiung 840, Taiwan, R.O.C.
            [10 ]Department of Biological Science and Technology, China Medical University, Taichung 404, Taiwan, R.O.C.
            [11 ]Department of Biotechnology, Asia University, Taichung 404, Taiwan, R.O.C.
            Author notes
            Correspondence to: Professor Jing Gung Chung, Department of Biological Science and Technology, China Medical University, 91 Hsueh Shih Road, Taichung 404, Taiwan, R.O.C., E mail: jgchung@ 123456mail.cmu.edu.tw
            Professor Lung Yuan Wu, School of Chinese Medicine for Post Baccalaureate, I Shou University, 8 Yida Road, Yanchao, Kaohsiung 840, Taiwan, R.O.C., E mail: dr.wuly@ 123456gmail.com
            [*]

            Contributed equally

            Journal
            Mol Med Rep
            Mol Med Rep
            Molecular Medicine Reports
            D.A. Spandidos
            1791-2997
            1791-3004
            July 2015
            09 March 2015
            09 March 2015
            : 12
            : 1
            : 133-140
            25760985 4438976 10.3892/mmr.2015.3454 mmr-12-01-0133
            Copyright © 2015, Spandidos Publications

            This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

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