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Single cell sequencing of gastric cancer and adjacent normal tissues

ABSTRACT: In this study, we used single-cell RNA sequencing (scRNA-seq) to further elucidate the composition of the gastric cancer and adjacent normal tissue microenvironment and found that TNF and ACTG1 may be key regulators of regulatory T cells (Tregs) in gastric cancer. A total of seven cell types were identified, including B cells, T cells, NK cells, mast cells, fibroblasts, endothelial cells, and epithelial cells. T cells were further divided into 8 subgroups. Among them, Tregs showed the greatest difference between GC and adjacent normal tissues. Next, we clarified the function and signaling pathway of Tregs in the GC tumor microenvironment, obtained the key regulatory proteins TNF and ACTG1, and explored their clinical significance and possible effects on Tregs in the GC tumor microenvironment. This scRNA-seq study may reveal the composition of tumor microenvironment and clarify the role of Tregs in the development of gastric cancer, providing new methods for GC treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE184198 | GEO | 2022/11/23

REPOSITORIES: GEO

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Project description:The better prognosis of patients with Epstein-Barr virus-positive gastric carcinoma than those with EBV-negative GC is correlated with the degree of recruitment of inflammatory tumor infiltrating cells (TIL) to the vicinity of tumor cells. We hypothesized that the better prognosis would associate with less genetic or epigenetic alterations in EBV(+)GC, or EBV infection should deregulate immune modulator proteins, of which secretion recruit TIL. Therefore we performed mRNA expression profilings in EBV(-)GC and EBV(+)GC, each of which was pair wise compared with their normal control. We found that EBV(+)GC had much more molecular homogeneity with focused alterations in immune modulator genes; The Pearson correlation matrix analyses demonstrated that EBV(+)GC tumor showed remarkably high tumor homogeneity. While EBV(-)GC had considerable number genes that are differentially expressed genes from their normal counterparts, EBV(+)GC showed only a handful, almost 20 fold less number of DEG than EBV(-)GC under the same p value cutoff (p<0.001). Gene ontology and pathway analyses showed that while pathways of cation homeostasis, digestion and ion transport were commonly deregulated in both GC types, genes for chromatin assembly, prostaglandin receptor activity, pattern specification process are selectively deregulated in EBV(-)GC tumors. In contrast, pathways or genes for cytokine activity, immune response and lipoprotein particle clearance are selectively deregulated in EBV(+)GC tumors. These results demonstrate that EBV(+)GC inherently evolves to high homogeneity with fewer changes in gene expression and these secret immune modulatory chemokines could recruit reactive immune cells to EBV(+)GC, leading to favorable microenvironment for cancer suppression. All patients underwent the surgery for advanced gastric carcinoma (GC) except one patient with early GC. The EBV-presence in the GC was verified by in situ EBV-encoded small RNA (ERER) staining.. The 14 paired EBV(-)GC patients and 12 paired EBV(+)GC patients were selected for this study. Tumor tissue (T)and normal tissues (N) from distant sites from tumor areas were dissected, frozen at -80C and were subjected to RNA purification, mRNA array profiling analyses.

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Single cell sequencing of gastric cancer and adjacent normal tissues

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