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Heterogeneity and chimerism of endothelial cells revealed by single cell transcriptome in orthotopic liver tumors

ABSTRACT: Heterogeneity and chimerism of endothelial cells revealed by single cell transcriptome in orthotopic liver tumors

PROVIDER: PRJNA631541 | ENA |

REPOSITORIES: ENA

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Heterogeneity and chimerism of endothelial cells revealed by single cell transcriptome in orthotopic liver tumors

Project description:To understand endothelial cell heterogeneity in naïve liver as well as in adjacent normal and liver tumor tissue. The single cells were profiled by single cell RNAseq.

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Heterogeneity and chimerism of endothelial cells revealed by single-cell transcriptome in orthotopic liver tumors.

Project description:The liver is a common host organ for cancer, either through lesions that arise in liver epithelial cells [e.g., hepatocellular carcinoma (HCC)] or as a site of metastasis by tumors arising in other organs (e.g., colorectal cancer). However, the changes that occur in liver stromal cells in response to cancer have not been fully characterized, nor has it been determined whether the different sources of liver cancer induce distinct stromal changes. Here, we performed single-cell profiling of liver stromal cells from mouse models of induced spontaneous liver cancer or implanted colorectal liver metastases, with a focus on tumor endothelial cells (ECs). While ECs in liver tissue adjacent to cancerous lesions (so-called adjacent normal) corresponded to liver zonation phenotypes, their transcriptomes were also clearly altered by the presence of a tumor. In comparison, tumor EC transcriptomes show stronger similarities to venous than sinusoidal ECs. Further, tumor ECs, independent of tumor origin, formed distinct clusters displaying conserved "tip-like" or "stalk-like" characteristics, similar to ECs from subcutaneous tumors. However, they also carried liver-specific signatures found in normal liver ECs, suggesting an influence of the host organ on tumor ECs. Our results document gene expression signatures in ECs in liver cancer and show that the host organ, and not the site of tumor origin (liver versus colorectal), is a primary determinant of EC phenotype. In addition, primarily in tumors, we further defined a cluster of chimeric cells that expressed both myeloid and endothelial cell markers and might play a role in tumor angiogenesis.

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Expression data from the orthotopic tumors of MES-SA

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