Purpose <p>Colorectal cancer (CRC) is the most common malignant tumor with a persistently high mortality rate worldwide. This study aimed to explore the anti-CRC effect and mechanisms of <i>Ruditapes philippinarum</i> polysaccharides (RPP).</p> Methods <p>We used HT-29 cells and HT-29 tumor-bearing mice to study the anti-CRC effects and mechanisms of RPP <i>in vitro</i> and <i>in vivo</i>.</p> Results <p>Animal experiments demonstrated that RPP-treated groups increased expression levels of Bax and cleaved caspase-3 proteins while reducing expression levels of Bcl-2 and Clusterin proteins in mice bearing HT-29 tumors. These results suggested the potential involvement of the mitochondrial apoptotic pathway in HT-29 cells apoptosis. Meanwhile, expression levels of <i>β</i>-catenin and its subsequent target proteins, such as Survivin, C-myc, and Cyclin D1, were suppressed, suggesting that RPP arrested the cell cycle of HT-29 cells in the G0/G1 phase by inhibiting the Wnt/<i>β</i>-catenin pathway. Additionally, RPP suppressed levels of TNF-<i>α</i>, IL-6, and IL-1<i>β</i>, and then alleviated the inflammatory response.</p> Conclusion <p>Overall, these findings could provide a new insight that RPP are promising polysaccharides to combat CRC as drugs or preventive health products.</p>

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Anti-colorectal cancer effect and mechanism of a polysaccharide from Ruditapes philippinarum

  • Xinyu Zhang,
  • Mengyue Liu,
  • Xuemei Zhang,
  • Zubo Du,
  • Yuxi Wei,
  • Fei Li

摘要

Purpose

Colorectal cancer (CRC) is the most common malignant tumor with a persistently high mortality rate worldwide. This study aimed to explore the anti-CRC effect and mechanisms of Ruditapes philippinarum polysaccharides (RPP).

Methods

We used HT-29 cells and HT-29 tumor-bearing mice to study the anti-CRC effects and mechanisms of RPP in vitro and in vivo.

Results

Animal experiments demonstrated that RPP-treated groups increased expression levels of Bax and cleaved caspase-3 proteins while reducing expression levels of Bcl-2 and Clusterin proteins in mice bearing HT-29 tumors. These results suggested the potential involvement of the mitochondrial apoptotic pathway in HT-29 cells apoptosis. Meanwhile, expression levels of β-catenin and its subsequent target proteins, such as Survivin, C-myc, and Cyclin D1, were suppressed, suggesting that RPP arrested the cell cycle of HT-29 cells in the G0/G1 phase by inhibiting the Wnt/β-catenin pathway. Additionally, RPP suppressed levels of TNF-α, IL-6, and IL-1β, and then alleviated the inflammatory response.

Conclusion

Overall, these findings could provide a new insight that RPP are promising polysaccharides to combat CRC as drugs or preventive health products.