期刊
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
卷 1872, 期 2, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.bbcan.2019.07.004
关键词
Gastric adenocarcinoma; Lactate; Carcinogenesis; Microbiota; Tumor microenvironment
资金
- National Health and Medical Research Council, Australia Early Career fellowship [APP1111461]
- Cancer Australia Priority-driven Collaborative Cancer Research grant [1129488]
- Cancer Institute NSW Career Development Fellowship [15/CDF/1-11]
- Ministry of Higher Education, Malaysia [UM.C/625/HIR/MOHE/CHAN/13/1]
- University of New South Wales
While Helicobacter pylori is a fundamental risk factor, gastric cancer (GC) aetiology involves combined effects of microbial (both H. pylori and non-H. pylori), host and environmental factors. Significant differences exist between the gastric microbiome of those with gastritis, intestinal metaplasia and GC, suggesting that dysbiosis in the stomach is dynamic and correlates with progression to GC. Most notably, a consistent increase in abundance of lactic acid bacteria (LAB) has been observed in GC patients including Streptococcus, Lactobacillus, Bifidobacterium and Lactococcus. This review summarises how LAB can influence GC by a number of mechanisms that include supply of exogenous lactate -a fuel source for cancer cells that promotes inflammation, angiogenesis, metastasis, epithelial-mesenchymal transition and immune evasion-, production of reactive oxygen species and N-nitroso compounds, as well as anti-H. pylori properties that enable colonization by other non-H. pylori carcinogenic pathobionts.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据