Department of Gastrointestinal Cancer Biology, Tianjin Medical University Cancer Institute & Hospital, Tianjin, 300060, China.
National Clinical Research Center for Cancer, Tianjin, 300060, China.
Cell Oncol (Dordr). 2021 Jun;44(3):701-714. doi: 10.1007/s13402-021-00596-y. Epub 2021 Mar 26.
The purpose of this study was to characterize alterations in mucosa-associated microbiota in different anatomical locations of the stomach during gastric cancer progression and to identify associations between Helicobacter pylori infection and gastric microbial changes in patients with gastric cancer.
Twenty-five H. pylori negative subjects with chronic gastritis and thirty-four subjects with gastric cancer were recruited, including H. pylori negative and positive patients with tumors in the antrum and the corpus. Gastric mucosa-associated microbiota were determined by 16S ribosomal RNA gene sequencing using a 454 sequencing platform.
We found that individuals with chronic gastritis from three different anatomical sites exhibited different microbiota compositions, although the microbial alpha diversity, richness and beta diversity were similar. Compared to patients with chronic gastritis, the gastric microbiota compositions were significantly different at the order level in the antrum and the corpus of patients with gastric cancer, which was dependent on the H. pylori infection status. Microbial alpha diversity and species richness, however, were similar between chronic gastritis and gastric cancer cases and independent of H. pylori status. The microbial community structure in patients with gastric cancer was distinct from that in patients with chronic gastritis. In addition, we found that the presence of H. pylori markedly altered the structure in gastric corpus cancer, but only mildly affected the antrum.
Our data revealed distinct niche-specific microbiota alterations during the progression from gastritis to gastric cancer. These alterations may reflect adaptions of the microbiota to the diverse specific environmental habitats in the stomach, and may play an important, as yet undetermined, role in gastric carcinogenesis.
本研究旨在描述胃癌进展过程中胃不同解剖部位黏膜相关微生物群的变化，并确定幽门螺杆菌（H. pylori）感染与胃癌患者胃微生物变化之间的关系。
招募了 25 名 H. pylori 阴性的慢性胃炎患者和 34 名胃癌患者，包括 H. pylori 阴性和阳性的肿瘤位于胃窦和胃体的患者。使用 454 测序平台，通过 16S 核糖体 RNA 基因测序来确定胃黏膜相关微生物群。
我们发现，来自三个不同解剖部位的慢性胃炎患者表现出不同的微生物群落组成，尽管微生物的α多样性、丰富度和β多样性相似。与慢性胃炎患者相比，胃癌患者胃窦和胃体的微生物群落组成在属水平上存在显著差异，这取决于 H. pylori 的感染状态。然而，慢性胃炎和胃癌患者之间的微生物α多样性和物种丰富度相似，且与 H. pylori 状态无关。胃癌患者的微生物群落结构与慢性胃炎患者明显不同。此外，我们发现 H. pylori 的存在显著改变了胃体癌的结构，但对胃窦的影响较小。
我们的数据揭示了从胃炎到胃癌进展过程中特定部位的微生物群落明显变化。这些变化可能反映了微生物对胃内不同特定环境生境的适应性，并且可能在胃癌发生中发挥重要但尚未确定的作用。
