Scholarlink

Background <p>Liver metastasis of colorectal cancer (CRC) remains a major clinical challenge, closely linked to poor prognosis and limited therapeutic efficacy. Emerging evidence implicates the gut microbiota in orchestrating the formation and maturation of the hepatic pre-metastatic niche (PMN) through the gut–liver axis.</p> Main body <p>Dysbiosis-induced disruption of intestinal barrier integrity facilitates microbial translocation, which triggers hepatic inflammation, immune suppression, metabolic reprogramming, and vascular remodelling, together creating a permissive soil for metastatic seeding. Among pathogenic taxa, <i>Fusobacterium nucleatum</i> has emerged as a key driver because it persistently colonises both primary tumours and hepatic metastases while modulating immunotolerance and chemoresistance. Therapeutically, narrow-spectrum antimicrobial approaches that target pro-metastatic taxa show promise for safely and selectively correcting microbiota-mediated PMN formation. In addition, faecal microbiota transplantation (FMT) combined with immune checkpoint inhibitors and anti-angiogenic therapy has yielded encouraging responses in refractory metastatic CRC by boosting anti-tumour immunity and restoring hepatic microvascular architecture.</p> Conclusion <p>Future research should integrate multidimensional biomarker assessment with personalised, microbiota-based therapeutic frameworks to achieve effective and durable prevention of CRC liver metastasis.</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

Gut microbiota-driven pre-metastatic niche formation in colorectal cancer liver metastasis: mechanisms and translational significance

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月21日

查看全文
  • Pengyu Chen,
  • Qian Geng,
  • Wenyu Zhu,
  • Hua Jiang

摘要

Background

Liver metastasis of colorectal cancer (CRC) remains a major clinical challenge, closely linked to poor prognosis and limited therapeutic efficacy. Emerging evidence implicates the gut microbiota in orchestrating the formation and maturation of the hepatic pre-metastatic niche (PMN) through the gut–liver axis.

Main body

Dysbiosis-induced disruption of intestinal barrier integrity facilitates microbial translocation, which triggers hepatic inflammation, immune suppression, metabolic reprogramming, and vascular remodelling, together creating a permissive soil for metastatic seeding. Among pathogenic taxa, Fusobacterium nucleatum has emerged as a key driver because it persistently colonises both primary tumours and hepatic metastases while modulating immunotolerance and chemoresistance. Therapeutically, narrow-spectrum antimicrobial approaches that target pro-metastatic taxa show promise for safely and selectively correcting microbiota-mediated PMN formation. In addition, faecal microbiota transplantation (FMT) combined with immune checkpoint inhibitors and anti-angiogenic therapy has yielded encouraging responses in refractory metastatic CRC by boosting anti-tumour immunity and restoring hepatic microvascular architecture.

Conclusion

Future research should integrate multidimensional biomarker assessment with personalised, microbiota-based therapeutic frameworks to achieve effective and durable prevention of CRC liver metastasis.