, Volume 46, Issue 6, pp 338-344

Polysaccharide K induces Mn superoxide dismutase (Mn-SOD) in tumor tissues and inhibits malignant progression of QR-32 tumor cells: possible roles of interferon α, tumor necrosis factor α and transforming growth factor β in Mn-SOD induction by polysaccharide K

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access

Abstract

 Previously we reported the malignant progression of QR-32, a regressor-type tumor clone, following co-implantation with foreign bodies (gelatin sponge or plastic plate) in normal syngeneic C57BL/6 mice. We also reported that the progression of QR-32 cells by a gelatin sponge was significantly inhibited in the mice administered polysaccharide K (PSK) and that PSK induced an increase of radical scavengers, especially manganese superoxide dismutase (Mn-SOD), locally at the site of tumor tissues. In this study, to reveal the possible mechanism by which PSK induced Mn-SOD in the tumor tissues, we examined the mRNA expression and protein levels of inflammatory cytokines in the tissues. We found that mRNAs of tumor necrosis factor α (TNFα) and interleukin-1α (IL-1α) were considerably expressed in both PSK-treated and phosphate-buffered-saline-treated tumors, and that the mRNA expression and protein level of interferon γ (IFNγ) increased in the tumor tissues treated with PSK. In vitro treatment of QR-32 cells with IFNγ did not significantly increase the production of Mn-SOD; however, the combination of IFNγ with TNFα increased the Mn-SOD production more effectively than did any of the cytokines used singly. Furthermore, we observed the down-regulation of the mRNA expression and protein level of transforming growth factor β (TGFβ) in the tumor tissues treated with PSK, and that in vitro treatment of QR-32 cells with TGFβ decreased the production of Mn-SOD. These results suggest that PSK suppresses the progression of QR-32 cells by increasing Mn-SOD via the modulation of inflammatory cytokines; that is, by decreasing TGF-β and increasing IFN-γ.

Received: 7 October 1997 / Accepted: 31 March 1998