Dual Effects of Intratumoral Microbial Metabolism on Tumors
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摘要: 研究已证实，肿瘤组织内部并不是无菌状态，而是定植着具有肿瘤特异性的微生物群落。这些瘤内微生物不仅自身能直接促进或抑制肿瘤，还可以通过活跃的代谢活动，影响肿瘤的发生发展及治疗响应。本文分别从促肿瘤与抗肿瘤两个角度，综述瘤内微生物代谢对肿瘤的作用及其机制，总结基于瘤内微生物代谢的肿瘤防治新策略。瘤内微生物代谢对肿瘤的精准调控网络仍需深入研究，解析其对肿瘤的双重效应及分子机制，有望为肿瘤防治提供新方向。Abstract: Research has confirmed that tumor tissues are not in a sterile state, but rather host microbial communities with tumor-specific characteristics. These intratumoral microorganisms not only directly promote or inhibit tumorigenesis themselves, but can also influence tumor development and therapeutic responses through their active metabolic activities. This review examines the effects and mechanisms of intratumoral microbial metabolism on tumors from both pro-tumoral and anti-tumoral perspectives, and summarizes novel strategies for tumor prevention and treatment based on intratumoral microbial metabolism. The precise regulatory network of intratumoral microbial metabolism on tumors requires further investigation. Elucidating its dual effects and molecular mechanisms on tumors is expected to provide new directions for tumor prevention and treatment.
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Key words:
- Intratumoral microbiota /
- Metabolism /
- Tumor /
- Therapy
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图 1 瘤内微生物代谢促肿瘤和抗肿瘤的机制（用BioRender网站自制）
注：Treg：调节性T细胞；TAMs：肿瘤相关巨噬细胞；CISD1：CDGSH铁硫结构域1；DC cell：树突细胞；IL-12：白介素-12；TNF-α：肿瘤坏死因子α；PD-1：细胞程序性死亡因子-1； tumor cell proliferation：肿瘤增殖；tumor metastasis：肿瘤转移；DNA damaging：DNA损伤；immunosuppressive microenvironment：免疫抑制微环境；immune activation and remodeling：免疫激活和重塑；CD8+ T cell exhaustion：CD8+ T细胞耗竭。
Figure 1. Pro-tumorigenic and anti-tumorigenic mechanisms of intratumoral microbiota metabolism （Created in BioRender.com）
图 2 “代谢-免疫-肿瘤”互作网络综合示意图（用BioRender网站自制）
注：Butyric acid：丁酸；HDAC2：组蛋白去乙酰化酶2；TAMs：肿瘤相关巨噬细胞；4-hydroxyphenylacetic acid：4-羟基苯乙酸；JAK2：非受体型酪氨酸蛋白激酶2；STAT3：信号转导及转录激活因子3；CXCL3：CXC趋化因子配体3；Ornithine：鸟氨酸；Formic acid：甲酸；AhR：芳烃受体；P-methylphenyl：对甲酚；ROS：活性氧；Kyn：犬尿氨酸；ILA：吲哚-3-乳酸；IAA：吲哚-3-乙酸；HDAC3：组蛋白去乙酰化酶3；TBX21：T-盒转录因子21；Exopolysaccharide：胞外多糖；TLR2：Toll样受体2；MyD88：骨髓分化因子88；DC：树突细胞；IL-12：白介素-12；TNF-α：肿瘤坏死因子α； 6-hydroxy caproic acid：6-羟基己酸；acetyl-CoA：乙酰辅酶A；RORC：RAR相关孤儿受体C；NEDD4L：神经前体细胞表达发育下调4L蛋白；TRF：铁转运蛋白；NK：自然杀伤细胞。
Figure 2. Schematic diagram of metabolism-immunity-tumor interaction network.（Created in BioRender.com）
表 1 瘤内微生物代谢促肿瘤机制汇总
Table 1. Mechanisms mediated by intratumoral microbiota metabolism
微生物种类 代谢产物 核心机制 生物学效应 链球菌、葡萄球菌 棕榈酸 结合CD36受体 促进肿瘤细胞增殖 大肠杆菌、志贺菌 脂多糖 激活NF-κB信号通路 促进肿瘤细胞增殖 戈登氏菌 溶血磷脂酰胆碱 激活JNK/ERK信号通路 促进肿瘤细胞增殖 空肠弯曲菌 细胞致死性膨胀毒素 激活JAK2/STAT3信号通路 促进肿瘤转移 牙周梭杆菌 棕榈酸 激活PI3K/AKT信号通路 促进肿瘤转移 鲍曼不动杆菌 烟碱酸 重编程肿瘤细胞代谢 促进肿瘤转移 具核梭杆菌 DL-同型半胱氨酸等 直接破坏DNA结构 DNA损伤 大肠杆菌 （pks+） 大肠杆菌素 直接破坏DNA结构 DNA断裂 新型福氏志贺菌 环二肽 直接破坏DNA结构 DNA损伤 齿垢放线菌 脂磷壁酸 诱导ROS过量蓄积 DNA断裂 脆弱拟杆菌 脆弱拟杆菌毒素 诱导ROS过量蓄积 DNA断裂 γ-变形菌 腐胺及琥珀酸 诱导ROS过量蓄积 DNA断裂 具核梭杆菌 甲酸 激活AhR信号通路 促进Th17细胞浸润 咽峡炎链球菌 鸟氨酸 抑制CD8+T细胞分化 免疫抑制 微小微单胞菌 对甲酚 提升组织ROS水平 诱导FOXP3+ Treg细胞分化 罗氏菌 丁酸 抑制HDAC2，上调H19 促进TAMs向M2型极化 注：NF-κB：核因子κB；JNK：c-Jun氨基末端激酶；ERK：胞外信号调节蛋白激酶；JAK2：非受体型酪氨酸蛋白激酶2；STAT3：信号转导及转录激活因子3；PI3K：磷脂酰肌醇3激酶；AKT：蛋白激酶B；ROS：活性氧；AhR：芳烃受体；HDAC2：组蛋白去乙酰化酶2；TAMs：肿瘤相关巨噬细胞。 
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表 2 瘤内微生物代谢抗肿瘤机制汇总
Table 2. Mechanisms mediated by intratumoral microbiota metabolism
微生物种类 代谢产物 核心机制 生物学效应 子宫内膜癌内菌群 丁酸 下调CISD1 诱导肿瘤细胞铁死亡 副干酪乳酸杆菌 吲哚-3-乙酸 阻断NF-κB信号通路 抑制肿瘤细胞增殖 双歧杆菌 胞外多糖 结合TLR2，招募MyD88 促进树突细胞分泌抗肿瘤细胞因子 经黏液真杆菌 6-羟基己酸 激活JAK/STAT信号通路 诱导TAMs向M1型极化 短小短芽孢杆菌 乙酰辅酶A 促进RORC乙酰化，增强NEDD4L表达 抑制NK细胞铁死亡 乳酸杆菌 吲哚-3-羧酸 促进犬尿氨酸生成 抑制Treg细胞分化，增强CD8+T细胞功能 罗伊氏乳杆菌 吲哚-3-乳酸 促进犬尿氨酸生成 抑制Treg细胞分化，增强CD8+T细胞功能 具核梭杆菌 丁酸 抑制HDAC3，激活TBX21，抑制PD-1表达 减轻CD8+T细胞耗竭 双歧杆菌 吲哚-3-乙酸 激活AhR信号通路，抑制IL-6表达 诱导TAMs向M1型极化，增强CD8+T细胞功能 注：CISD1：CDGSH铁硫结构域1基因；NF-κB：核因子κB；MyD88：骨髓分化因子88；JAK：非受体型酪氨酸蛋白激酶；STAT：信号转导及转录激活因子；RORC：RAR相关孤儿受体C；NEDD4L：神经前体细胞表达发育下调4L蛋白；HDAC3：组蛋白去乙酰化酶3；TBX21：组蛋白去乙酰化酶3；AhR：芳烃受体；IL-6：白介素-6；TAMs：肿瘤相关巨噬细胞。
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