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作者

Zhongchao Li, Mingming Li, Yue Yang, Zhicheng Sun, Zhibin Chang, Yunsong Chen, Lei Zhao

作者单位

Affiliations ¹ Shandong University Cancer Center, Jinan, Shandong, China. ² Department of Hepatobiliary Surgery, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China. ³ Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China. ⁴ The Affiliated Cancer Hospital of Xinjiang Medical University, Urumqi, China.

刊名

Journal of cancer research and therapeutics

年份

2025

ISSN

1998-4138

关键词

Colorectal cancer commensal dysbiosis liver metastasis tumor microenvironment tumor-associated macrophages.

摘要

Background: Gut microorganisms are involved in the occurrence and progression of various types of cancer, including colorectal cancer. Previous studies have shown that the disruption of commensal homeostasis can promote tumor metastasis. The present study aimed to investigate the effects of gut commensal dysbiosis on the risk of colorectal cancer liver metastasis and its mechanisms. Materials and methods: A mouse model of CRLM with the commensal dysbiosis background was established. This model ...更多

Background: Gut microorganisms are involved in the occurrence and progression of various types of cancer, including colorectal cancer. Previous studies have shown that the disruption of commensal homeostasis can promote tumor metastasis. The present study aimed to investigate the effects of gut commensal dysbiosis on the risk of colorectal cancer liver metastasis and its mechanisms. Materials and methods: A mouse model of CRLM with the commensal dysbiosis background was established. This model was used to investigate the impact of commensal dysbiosis on CRLM. Results: Commensal dysbiosis promoted CRLM development via the C-C chemokine ligand 6 and C-C chemokine receptor 1 axis. Moreover, it altered the liver tumor microenvironment by recruiting tumor-associated macrophages , notably M2-like TAMs, and promoted liver metastasis growth. Liver metastasis was promoted via the upregulation of CCL6 expression levels, which resulted in CCR1+TAM infiltration into the TME. Notably, inhibiting CCR1 expression could reduce CRLM. Conclusion: Commensal dysbiosis could promote CRLM development via CCL6/CCR1 signaling. Targeting this signaling axis could be an effective method to inhibit CRLM by regulating the TME.收起

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