Iguchi C, Nio Y, Takeda H, Yamasawa K, Hirahara N, Toga T, Itakura M, Tamura K
First Department of Surgery, Shimane Medical University, 89-1, Enya-cho, Izumo, Shimane 693-8501, Japan.
Anticancer Res. 2001 Mar-Apr;21(2A):1007-13.
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.
PSK是一种植物多糖，在日本和其他亚洲国家被广泛用于癌症免疫治疗。人们认为其抗肿瘤作用源于对荷瘤宿主的免疫调节活性。本研究旨在评估PSK对人KATO-3胃癌细胞系和Colo205结肠癌细胞系体外增殖和侵袭的直接作用，以及这些细胞表面分子如HLA和黏附分子的表达。培养开始48小时后，100微克/毫升的PSK显著抑制KATO-3细胞的体外生长，培养开始24小时后，10和100微克/毫升的PSK显著抑制Colo205细胞的体外生长。用基质胶侵袭小室评估PSK对肿瘤细胞体外侵袭的影响，结果显示，PSK浓度分别超过10微克/毫升和5微克/毫升时，KATO-3和Colo205细胞的侵袭受到抑制。KATO-3细胞非常微弱地表达HLA-ABC、HLA-A2/A28、HLA-DR，几乎处于基线水平，但HLA-B27、β2微球蛋白和HLA-DQ以不同水平表达。用PSK处理KATO-3细胞后，HLA-B27和β2微球蛋白的表达显著增强。Colo205细胞以不同水平表达本研究中检测的所有I类抗原，但II类抗原几乎处于基线水平。PSK也增强了Colo205细胞上I类抗原的表达。ICAM-1在KATO-3细胞上表达，但在Colo205细胞上不表达。与100微克/毫升的PSK相比，10微克/毫升的PSK处理使ICAM-1的表达增强程度更大。腺癌抗原AC-81在两种细胞系上均强烈表达，但PSK处理显著增强了其表达。这些结果表明，PSK处理后肿瘤细胞上HLA I类表达的增强可能是PSK诱导抗肿瘤免疫的机制之一。
