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Single cell analysis of tumors developed from mouse dysplastic stem cells

ABSTRACT: To investigate whether the CD44v6neg/CD133+/CD166+ dysplastic stem cells are responsible for gastric adenocarcinoma development and cancer cell heterogeneity in the stomach, we used single cell RNA-seq (scRNA-seq) to examine gene expression profiles of heterogenous cancer cells in two types of gastric adenocarcinoma, cystic type and tubular type, developed from the dysplastic stem cell injection under the skin of immunodeficient nude mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE202192 | GEO | 2022/09/28

REPOSITORIES: GEO

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Comparison of transcriptomic profiles between dysplastic stem cell subpopulations

Project description:To investigate transcriptomic profiles of of two dysplastic stem cell (DSC) subpopulations, CD44v6neg/CD133+/CD166+ (DP-DSC) and CD44v6+/CD133+/CD166+ (TP-DSC), in dysplastic organoids (Meta4 organoids) established from active-Kras induced mouse stomachs

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Single cell analysis of tumors developed from mouse dysplastic stem cells

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Project description:Background: The risk of developing Barrett’s esophagus (BE) and/or esophageal adenocarcinoma (EAC) is associated with specific demographic and behavioral factors, including gender, obesity/elevated body-mass index (BMI), and tobacco use. Alterations in DNA methylation, an epigenetic modification that can affect gene expression and that can be influenced by environmental factors, is frequently present in both BE and EAC and is believed to play a role in the formation of BE and its progression to EAC. It is currently unknown whether obesity or tobacco smoking influence the risk of developing BE/EAC via the induction of alterations in DNA methylation. To investigate this possibility, we assessed the genome-wide methylation status of 81 esophageal tissues, including BE, dysplastic BE, and EAC epithelia using HumanMethylation450 BeadChips (Illumina). Results: We found numerous differentially methylated loci in the esophagus tissues when comparing males to females, obese to lean individuals, and smokers to nonsmokers. Differences in DNA methylation between these groups were seen in a variety of functional genomic regions, and both within and outside of CpG islands. Several cancer-related pathways were found to have differentially methylated genes between these comparison groups. Conclusions: Our findings suggest obesity and tobacco smoking may influence DNA methylation in the esophagus and raise the possibility that these risk factors affect the development of BE, dysplastic BE, and EAC through influencing the epigenetic status of specific loci that have a biologically plausible role in cancer formation.

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