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- Title
Polysaccharide-K (PSK) may suppress surgical stress-induced metastasis in rat colon cancer.
- Authors
Tamagawa, Koji; Horiuchi, Tetsuya; Wada, Tsutomu; Bannai, Kenji; Ando, Takao
- Abstract
Purpose: We previously demonstrated that hepatic ischemia and reperfusion (I/R) injury increased liver metastasis and cancer growth of RCN-H4 cells. Using a rat model of hepatic I/R-induced liver metastasis, we investigated the metastasis-suppressing effect of polysaccharide-K (PSK), a biological response modifier composed of protein-bound polysaccharide. Methods: Fischer rats underwent 60 min of 70% partial hepatic ischemia. After 60 min of reperfusion, rat colon adenocarcinoma cells (RCN-H4) were inoculated intrasplenically. PSK was administered orally before I/R, after I/R, or before and after I/R. The weights of metastatic lesions of the liver or the numbers of liver metastatic nodules were determined on day 21. The effect of PSK on angiogenesis was studied by a rat cornea model using RCN-H4 cells or a vascular endothelial growth factor (VEGF)-containing pellet and an in vitro VEGF-induced endothelial cell migration assay. Results: PSK administration significantly ( p < 0.05) suppressed the I/R-induced increase in hepatic metastasis of RCN-H4 cells. The suppression of I/R-promoted metastasis was observed irrespective of the timing of administration. Furthermore, PSK significantly suppressed angiogenesis induced by RCN-H4 cells ( p < 0.05) and the VEGF pellet ( p < 0.01). PSK significantly suppressed the VEGF-induced migration of vascular endothelial cells ( p < 0.05). Conclusion: PSK may suppress metastasis induced by hepatic I/R. The suppression of angiogenesis by PSK may be one of the mechanisms of the inhibition of hepatic metastasis.
- Subjects
POLYSACCHARIDES; ISCHEMIA; LIVER cancer; TUMOR growth; METASTASIS
- Publication
Langenbeck's Archives of Surgery, 2012, Vol 397, Issue 3, p475
- ISSN
1435-2443
- Publication type
Article
- DOI
10.1007/s00423-011-0896-2