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September 2012 Volume 4 Issue 3

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Article

Polysaccharide K suppresses angiogenesis in colon cancer cells

  • Authors:
    • Yoshiki Satoh
    • Takanori Goi
    • Toshiyuki Nakazawa
    • Youhei Kimura
    • Yasuo Hirono
    • Kanji Katayama
    • Akio Yamaguchi
  • View Affiliations / Copyright

    Affiliations: First Department of Surgery, University of Fukui, Yoshida-gun, Fukui, Japan
  • Pages: 370-374
    |
    Published online on: July 4, 2012
       https://doi.org/10.3892/etm.2012.632
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Abstract

The protein-bound polysaccharide K (PSK) is used as a non-specific immunotherapeutic agent for the treatment of colon cancer. Little research, however, has been conducted on its association with angiogenesis, which is a prognostic factor markedly correlated with hematogenous metastases. We therefore decided to investigate the action of PSK on angiogenic growth factors, angiogenesis inhibitors and angiogenesis in colon cancer cells. Reverse transcription-polymerase chain reaction (RT-PCR) was used to investigate changes in HIF-1α mRNA expression. PCR array was used to investigate changes in angiogenic growth factors and angiogenesis inhibitors, as well as the expression of related genes. Colon cancer cells were cultured with or without PSK for 48 h. The following day, cells were cultured for two days at 37˚C in new complete media. The resulting culture medium was placed in the chamber of a tube formation system in order to investigate tube formation. Investigation of HIF-1α mRNA expression in colon cancer cell lines and in cells cultured under identical conditions with added PSK revealed a significant decrease in expression, as well as a decrease in angiogenic growth factors and related genes in PSK-treated colon cancer cell lines. By contrast, levels of angiogenesis inhibitors and related genes were higher in the PSK-treated colon cancer cell lines. Investigation of tube formation revealed that elongation was inhibited in the medium of the PSK-treated colon cancer cell lines in comparison to the medium of the non-treated colon cancer cell lines. PSK suppresses angiogenic growth factors and related genes, enhances angiogenesis inhibitors and related genes and ultimately suppresses angiogenesis in colon cancer cells.
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Copy and paste a formatted citation
Spandidos Publications style
Satoh Y, Goi T, Nakazawa T, Kimura Y, Hirono Y, Katayama K and Yamaguchi A: Polysaccharide K suppresses angiogenesis in colon cancer cells. Exp Ther Med 4: 370-374, 2012.
APA
Satoh, Y., Goi, T., Nakazawa, T., Kimura, Y., Hirono, Y., Katayama, K., & Yamaguchi, A. (2012). Polysaccharide K suppresses angiogenesis in colon cancer cells. Experimental and Therapeutic Medicine, 4, 370-374. https://doi.org/10.3892/etm.2012.632
MLA
Satoh, Y., Goi, T., Nakazawa, T., Kimura, Y., Hirono, Y., Katayama, K., Yamaguchi, A."Polysaccharide K suppresses angiogenesis in colon cancer cells". Experimental and Therapeutic Medicine 4.3 (2012): 370-374.
Chicago
Satoh, Y., Goi, T., Nakazawa, T., Kimura, Y., Hirono, Y., Katayama, K., Yamaguchi, A."Polysaccharide K suppresses angiogenesis in colon cancer cells". Experimental and Therapeutic Medicine 4, no. 3 (2012): 370-374. https://doi.org/10.3892/etm.2012.632
Copy and paste a formatted citation
x
Spandidos Publications style
Satoh Y, Goi T, Nakazawa T, Kimura Y, Hirono Y, Katayama K and Yamaguchi A: Polysaccharide K suppresses angiogenesis in colon cancer cells. Exp Ther Med 4: 370-374, 2012.
APA
Satoh, Y., Goi, T., Nakazawa, T., Kimura, Y., Hirono, Y., Katayama, K., & Yamaguchi, A. (2012). Polysaccharide K suppresses angiogenesis in colon cancer cells. Experimental and Therapeutic Medicine, 4, 370-374. https://doi.org/10.3892/etm.2012.632
MLA
Satoh, Y., Goi, T., Nakazawa, T., Kimura, Y., Hirono, Y., Katayama, K., Yamaguchi, A."Polysaccharide K suppresses angiogenesis in colon cancer cells". Experimental and Therapeutic Medicine 4.3 (2012): 370-374.
Chicago
Satoh, Y., Goi, T., Nakazawa, T., Kimura, Y., Hirono, Y., Katayama, K., Yamaguchi, A."Polysaccharide K suppresses angiogenesis in colon cancer cells". Experimental and Therapeutic Medicine 4, no. 3 (2012): 370-374. https://doi.org/10.3892/etm.2012.632
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