肠道菌群与结直肠癌：从发病机制到治疗干预的研究进展

doi:10.12092/j.issn.1009-2501.2026.07.010

摘要/Abstract

摘要：

结直肠癌（colorectal cancer，CRC）是世界上最常见的癌症之一，近年来其发病率呈不断上升的趋势。对CRC开展的临床研究和在动物模型得到的实验证据将肠道菌群与CRC联系起来，肠道菌群作为CRC发生发展的关键调节因子，主要通过塑造局部免疫与炎症微环境、产生具有抑癌或促癌活性的代谢物，以及分泌基因毒性物质等多种机制，驱动CRC的发生发展。与此同时，肠道菌群也可通过多重机制影响CRC对化疗和免疫治疗的敏感性。本文旨在探讨与CRC发生发展以及治疗密切相关的特定菌群，重点介绍肠道菌群介导的CRC的发病机制以及目前有效的治疗手段，以期推动对肠道菌群与CRC更深层次关系的研究，并为提升CRC的疗效提供新的研究策略。

关键词: 结直肠癌, 肠道菌群, 化疗, 免疫治疗

Abstract:

Colorectal cancer (CRC) is one of the most prevalent malignancies worldwide, and its incidence has shown a steadily increasing trend in recent years. Clinical investigations and experimental evidence from animal models have established a strong association between the gut microbiota and CRC. The gut microbiota functions as a key regulatory factor in the initiation and progression of CRC, primarily through shaping the local immune and inflammatory microenvironment, producing metabolites with either tumor-suppressive or tumor-promoting activities, and secreting genotoxic substances, among other mechanisms, thereby driving CRC development. Meanwhile, the gut microbiota can also modulate the sensitivity of CRC to chemotherapy and immunotherapy through multiple pathways. This review aims to explore specific microbial taxa closely related to CRC onset, progression, and treatment, with a particular focus on the gut microbiota–mediated pathogenic mechanisms of CRC and currently effective therapeutic strategies. Ultimately, this work seeks to advance understanding of the deeper interplay between the gut microbiota and CRC, while providing novel perspectives for improving therapeutic efficacy in CRC.

Key words: colorectal cancer, gut microbiota, chemotherapy, immunotherapy

中图分类号:

R735.34

刘威, 张伟. 肠道菌群与结直肠癌：从发病机制到治疗干预的研究进展[J]. 中国临床药理学与治疗学, 2026, 31(7): 937-947.

Wei LIU, Wei ZHANG. Gut microbiota and colorectal cancer: advances from pathogenic mechanisms to therapeutic interventions[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2026, 31(7): 937-947.

图/表 4

参考文献 69

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Gut microbiota	Treatment	Mechanisms	References
F. nucleatum	Promote chemoresistance	F. nucleatum targets the TLR4-MyD88 signaling pathway to modulate autophagy.	[47]
B. fragilis	Promote chemoresistance	SusD/RagB, the surface protein of B. fragilis activates the Notch1 signaling pathway, suppressing chemotherapy-induced apoptosis.	[48]
Gut microbiota	Potentiate drug toxicity	Gut microbiota secrete β-glucuronidase to decouple SN-38G, leading to intestinal toxicity.	[50]
L. johnsonii	Promote anti-PD-1 efficacy	IPA produced in cooperation with C. sporogenes regulates the stemness program in CD8⁺T cells, potentiating Tpex generation.	[51]
R. intestinalis	Promote anti-PD-1 efficacy	Butyrates produced by R. intestinalis activate the NF-κB signaling pathway to enhance T cell function.	[52]
F. nucleatum	Promote anti-PD-1 efficacy	Butyric acid produced by F. nucleatum suppresses PD-1 gene transcription, ameliorating CD8⁺T cell exhaustion.	[53]
F. nucleatum	Promote anti-PD-L1 efficacy	F. nucleatum induces PD-L1 expression by activating STING signaling and increased the accumulation of (IFN-γ)⁺ CD8⁺ TILs.	[54]
F. nucleatum	Reduce anti-PD-1 efficacy	Succinate produced by F. nucleatum suppresses the cGAS-(IFN-β) pathway, limiting CD8⁺T cell infiltration in TME.	[55]
P. anaerobius	Reduce anti-PD-1 efficacy	P. anaerobius activates the NF-κB signaling to induce CXCL1 secretion, promoting MDSCs migration into tumors.	[56]
L. gallinarum	Promote anti-PD-1 efficacy	ICA derived from L. gallinarum targets the IDO1-Kyn-AHR axis, suppressing CD4⁺ Treg differentiation while enhancing CD8⁺T cell function.	[62]
L. rhamnosus GG	Promote anti-PD-1 efficacy	LGG triggers type I interferon production in DCs, enhancing the cross-priming of antitumour CD8⁺T cells	[64]
B. pseudolongum	Promote anti- CTLA-4 efficacy	L-arginine signaling through SLC7A1 reprograms CD8⁺T cells toward tissue-resident memory fate.	[67]

Gut microbiota	Treatment	Mechanisms	References
F. nucleatum	Promote chemoresistance	F. nucleatum targets the TLR4-MyD88 signaling pathway to modulate autophagy.	[47]
B. fragilis	Promote chemoresistance	SusD/RagB, the surface protein of B. fragilis activates the Notch1 signaling pathway, suppressing chemotherapy-induced apoptosis.	[48]
Gut microbiota	Potentiate drug toxicity	Gut microbiota secrete β-glucuronidase to decouple SN-38G, leading to intestinal toxicity.	[50]
L. johnsonii	Promote anti-PD-1 efficacy	IPA produced in cooperation with C. sporogenes regulates the stemness program in CD8⁺T cells, potentiating Tpex generation.	[51]
R. intestinalis	Promote anti-PD-1 efficacy	Butyrates produced by R. intestinalis activate the NF-κB signaling pathway to enhance T cell function.	[52]
F. nucleatum	Promote anti-PD-1 efficacy	Butyric acid produced by F. nucleatum suppresses PD-1 gene transcription, ameliorating CD8⁺T cell exhaustion.	[53]
F. nucleatum	Promote anti-PD-L1 efficacy	F. nucleatum induces PD-L1 expression by activating STING signaling and increased the accumulation of (IFN-γ)⁺ CD8⁺ TILs.	[54]
F. nucleatum	Reduce anti-PD-1 efficacy	Succinate produced by F. nucleatum suppresses the cGAS-(IFN-β) pathway, limiting CD8⁺T cell infiltration in TME.	[55]
P. anaerobius	Reduce anti-PD-1 efficacy	P. anaerobius activates the NF-κB signaling to induce CXCL1 secretion, promoting MDSCs migration into tumors.	[56]
L. gallinarum	Promote anti-PD-1 efficacy	ICA derived from L. gallinarum targets the IDO1-Kyn-AHR axis, suppressing CD4⁺ Treg differentiation while enhancing CD8⁺T cell function.	[62]
L. rhamnosus GG	Promote anti-PD-1 efficacy	LGG triggers type I interferon production in DCs, enhancing the cross-priming of antitumour CD8⁺T cells	[64]
B. pseudolongum	Promote anti- CTLA-4 efficacy	L-arginine signaling through SLC7A1 reprograms CD8⁺T cells toward tissue-resident memory fate.	[67]

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