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Dissecting the single-cell transcriptome network underlying gastric premalignant lesions and early gastric cancer [10x genomics]

ABSTRACT: Intestinal-type gastric cancer is preceded by premalignant lesions including chronic atrophic gastritis and intestinal metaplasia. In this study, we performed a scRNA-seq survey of 56,440 cells from thirteen gastric antral mucosa biopsies from nine patients with Non-atrophic gastritis (NAG), CAG, IM or early gastric cancer (EGC), and constructed a single-cell transcriptome atlas for gastric premalignant and early-malignant lesions. The thirteen biopsies, including three wild superficial gastritis (NAG) ones, three CAG ones, six IM ones and one EGC , spanned the cascade from gastritis to early gastric cancer.For each biopsy, we isolated single cells without prior selection for cell types and utilized the 10x Chromium platform to generate RNA-seq data. After removing low-quality cells (Methods), a total of 32, 332 cells that passed the quality control were retained for subsequent analysis, which yielded a median of 1941 detected genes per cell.

ORGANISM(S): Homo sapiens

PROVIDER: GSE134520 | GEO | 2019/07/20

REPOSITORIES: GEO

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Project description:Chronic infection with the bacterial pathogen Helicobacter pylori is a risk factor for the development of gastric cancer, yet remains asymptomatic in a majority of individuals. We report here that the C57Bl6 mouse model of experimental infection with the closely related H. felis recapitulates this wide range in host susceptibility. A majority of infected mice develop premalignant lesions such as gastric atrophy, compensatory epithelial hyperplasia and intestinal metaplasia, whereas a minority is completely protected from preneoplasia. Protection is associated with the failure to mount an IFN-gamma response to the infection and an associated high Helicobacter burden. We demonstrate that IFN-gamma is essential for clearance of Helicobacter, but also mediates the formation of preneoplastic lesions. We further provide evidence that IFN-gamma triggers a specific transcriptional program in murine gastric epithelial cells in vitro and in vivo, and induces their preferential transformation to the hyperplastic phenotype. In summary, our data suggest a dual role for IFN-gamma in Helicobacter pathogenesis that could provide an explanation for the differential susceptibility to H. pylori-induced gastric pathology in the human population. Keywords: response to in vitro stimulus / comparison of histopathological states We chose mice for gene expression profiling that following Helicobacter infection had (a) symptoms of gastritis, but no epithelial changes, (b) atrophic gastritis accompanied by corpus gland hyperplasia or (c) atrophic gastritis accompanied by intestinal metaplasia. An uninfected control group was also included in the analysis, as were two groups of mice that lacked mature T- and B-cells due to a deletion mutation in the rag1 gene (Rag-1-/-) and that were either experimentally infected or served as Rag-1-/- uninfected controls. To see the effects of IFNg on murine gastric epithelial cells we analysed an immortalized murine primary gastric epithelial cell line treated with three different concentrations of IFNg in comparison to an untreated control.

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Dissecting the single-cell transcriptome network underlying gastric premalignant lesions and early gastric cancer [10x genomics]

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