Plant polysaccharide PSK: cytostatic effects on growth and invasion; modulating effect on the expression of HLA and adhesion molecules on human gastric and colonic tumor cell surface.
PSK is a plant polysaccharide widely used for cancer immunotherapy in Japan and other Asian countries. It is considered that its antitumor effect is derived from its immunomodulating activity on the tumor-bearing host. The present study was designed to assess the direct action of PSK on in vitro proliferation and invasion of human KATO-3 gastric and Colo205 colonic cancer cell lines, and the expression of surface molecules such as HLA and adhesion molecules on these cells. The in vitro growth of KATO-3 cells was significantly inhibited by 100 micrograms/ml of PSK 48 hrs after culture initiation, and that of Colo205 was significantly inhibited by 10 and 100 micrograms/ml of PSK 24 hrs after culture initiation. The effect of PSK on the in vitro invasion of the tumor cells, assessed with a Matrigel invasion chamber, revealed that invasion of KATO-3 and Colo205 cells was inhibited by more than 10 micrograms/ml and more than 5 micrograms/ml of PSK, respectively. KATO-3 cells expressed HLA-ABC, HLA-A2/A28, HLA-DR very weakly, at almost baseline levels, but HLA-B27, B2-microglobulin and HLA-DQ were expressed at various levels. After treatment of KATO-3 cells with PSK, the expression of HLA-B27 and beta 2-microglobulin was significantly enhanced. Colo205 cells expressed all class-I antigens tested in this study at different levels, but class-II antigens at almost baseline levels. PSK also enhanced the expression of class-I antigens on Colo205 cells. ICAM-1 was expressed on KATO-3, but not on Colo205. The expression of ICAM-1 was enhanced to a greater extent by treatment with 10 micrograms/ml than with 100 micrograms/ml of PSK. Adenocarcinoma antigen AC-81 was strongly expressed on both cell lines, but PSK-treatment significantly enhanced its expression. These results suggested that enhancement of HLA class-I expression on tumor cells after PSK treatment may be one of the mechanisms responsible for the induction of anti-tumor immunity by PSK.
Iguchi
C
C
First Department of Surgery, Shimane Medical University, 89-1, Enya-cho, Izumo, Shimane 693-8501, Japan.
Nio
Y
Y
Takeda
H
H
Yamasawa
K
K
Hirahara
N
N
Toga
T
T
Itakura
M
M
Tamura
K
K
D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology*; D002455:Cell Division / Q000187:drug effects; D002462:Cell Membrane / Q000378:metabolism; D003110:Colonic Neoplasms; D006680:HLA Antigens / Q000096:biosynthesis*; D006683:HLA-DQ Antigens / Q000096:biosynthesis; D006684:HLA-DR Antigens / Q000096:biosynthesis; D015395:Histocompatibility Antigens Class I / Q000096:biosynthesis; D006801:Humans; D007155:Immunologic Factors / Q000494:pharmacology*; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis*; D016169:Lymphocyte Function-Associated Antigen-1 / Q000096:biosynthesis*; D009361:Neoplasm Invasiveness / Q000517:prevention & control*; D011509:Proteoglycans / Q000494:pharmacology*; D013274:Stomach Neoplasms; D014407:Tumor Cells, Cultured
D000972:Antineoplastic Agents, Phytogenic; D006680:HLA Antigens; D006683:HLA-DQ Antigens; D006684:HLA-DR Antigens; D015395:Histocompatibility Antigens Class I; D007155:Immunologic Factors; D016169:Lymphocyte Function-Associated Antigen-1; D011509:Proteoglycans; D018799:Intercellular Adhesion Molecule-1; C010770:polysaccharide-K