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肠道微生物群与胃肠道癌症:朋友还是敌人?

Gut microbiome in gastrointestinal cancer: a friend or foe?

机构信息

Department of Oncology, Shengjing Hospital of China Medical University, Shenyang, 110004, Liaoning province, China.

Department of Gastroenterological Surgery, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

出版信息

Int J Biol Sci. 2022 Jun 21;18(10):4101-4117. doi: 10.7150/ijbs.69331. eCollection 2022.

DOI:10.7150/ijbs.69331
PMID:35844804
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9274484/
Abstract

The impact of the gut microbiome on host health is becoming increasingly recognized. To date, there is growing evidence that the complex characteristics of the microbial community play key roles as potential biomarkers and predictors of responses in cancer therapy. Many studies have shown that altered commensal bacteria lead to cancer susceptibility and progression in diverse pathways. In this review, we critically assess the data for gut microbiota related to gastrointestinal cancer, including esophageal, gastric, pancreatic, colorectal cancer, hepatocellular carcinoma and cholangiocarcinoma. Importantly, the underlying mechanisms of gut microbiota involved in cancer occurrence, prevention and treatment are elucidated. The purpose of this review is to provide novel insights for applying this understanding to the development of new therapeutic strategies in gastrointestinal cancer by targeting the microbial community.

摘要

肠道微生物组对宿主健康的影响正日益受到重视。迄今为止,越来越多的证据表明,微生物群落的复杂特征在癌症治疗的反应中发挥着关键作用,可能成为潜在的生物标志物和预测因子。许多研究表明,共生细菌的改变导致了不同途径的癌症易感性和进展。在这篇综述中,我们批判性地评估了与胃肠道癌症相关的肠道微生物组数据,包括食管癌、胃癌、胰腺癌、结直肠癌、肝细胞癌和胆管癌。重要的是,阐明了肠道微生物群在癌症发生、预防和治疗中涉及的潜在机制。本综述的目的是为通过靶向微生物群落开发胃肠道癌症新的治疗策略提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e03d/9274484/753afee7c092/ijbsv18p4101g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e03d/9274484/acaa6d4f3141/ijbsv18p4101g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e03d/9274484/753afee7c092/ijbsv18p4101g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e03d/9274484/acaa6d4f3141/ijbsv18p4101g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e03d/9274484/cd7f5c839543/ijbsv18p4101g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e03d/9274484/4d412989e290/ijbsv18p4101g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e03d/9274484/753afee7c092/ijbsv18p4101g005.jpg

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Helicobacter pylori-induced RASAL2 Through Activation of Nuclear Factor-κB Promotes Gastric Tumorigenesis via β-catenin Signaling Axis.幽门螺杆菌诱导的 RASAL2 通过激活核因子-κB 通过 β-连环蛋白信号轴促进胃癌发生。
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Abundance and Metabolism Disruptions of Intratumoral Microbiota by Chemical and Physical Actions Unfreeze Tumor Treatment Resistance.化学和物理作用改变肿瘤内微生物群落的丰度和代谢紊乱,从而打破肿瘤治疗抵抗。
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