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Polysaccharide K suppresses angiogenesis in colon cancer cells
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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3503532/ https://www.ncbi.nlm.nih.gov/pubmed/23181101 http://dx.doi.org/10.3892/etm.2012.632 |
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author | SATOH, YOSHIKI GOI, TAKANORI NAKAZAWA, TOSHIYUKI KIMURA, YOUHEI HIRONO, YASUO KATAYAMA, KANJI YAMAGUCHI, AKIO |
author_facet | SATOH, YOSHIKI GOI, TAKANORI NAKAZAWA, TOSHIYUKI KIMURA, YOUHEI HIRONO, YASUO KATAYAMA, KANJI YAMAGUCHI, AKIO |
author_sort | SATOH, YOSHIKI |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3503532 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-35035322013-09-01 Polysaccharide K suppresses angiogenesis in colon cancer cells SATOH, YOSHIKI GOI, TAKANORI NAKAZAWA, TOSHIYUKI KIMURA, YOUHEI HIRONO, YASUO KATAYAMA, KANJI YAMAGUCHI, AKIO Exp Ther Med Articles 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. D.A. Spandidos 2012-09 2012-07-04 /pmc/articles/PMC3503532/ /pubmed/23181101 http://dx.doi.org/10.3892/etm.2012.632 Text en Copyright © 2012, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Articles SATOH, YOSHIKI GOI, TAKANORI NAKAZAWA, TOSHIYUKI KIMURA, YOUHEI HIRONO, YASUO KATAYAMA, KANJI YAMAGUCHI, AKIO Polysaccharide K suppresses angiogenesis in colon cancer cells |
title | Polysaccharide K suppresses angiogenesis in colon cancer cells |
title_full | Polysaccharide K suppresses angiogenesis in colon cancer cells |
title_fullStr | Polysaccharide K suppresses angiogenesis in colon cancer cells |
title_full_unstemmed | Polysaccharide K suppresses angiogenesis in colon cancer cells |
title_short | Polysaccharide K suppresses angiogenesis in colon cancer cells |
title_sort | polysaccharide k suppresses angiogenesis in colon cancer cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3503532/ https://www.ncbi.nlm.nih.gov/pubmed/23181101 http://dx.doi.org/10.3892/etm.2012.632 |
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