ArticleCancer immunology, immunotherapy : CII2024
Ly6E on tumor cells impairs anti-tumor T-cell responses: a novel mechanism of tumor-induced immune exclusion.
Article in Cancer immunology, immunotherapy : CII, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Unveiling the Importance of the Expression of LY6/UPAR Gene Family Members in Urothelial Carcinoma of the Urinary Bladder.Biomedicines · 2026Article
- Observational
- Identification and Validation of a Novel Theranostic Target in Triple Negative Breast Cancer with Transcriptomics and Protein Analyses.Breast cancer (Dove Medical Press) · 2026Article
- Silencing LY6K Suppresses CD44Current issues in molecular biology · 2024Article
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8 authors.
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Abstract
backgroundLymphocyte antigen 6 complex, locus E (Ly6E) has been initially demonstrated to involve in T cell activity and impair viral infectivity. Recently, high expression levels of Ly6E have been reported in tumor microenvironment (TME) of various types of cancers. However, the immunoregulatory mechanism of Ly6E manipulating TME remains unknown.
methodsTCGA database and Kaplan-Meier plotter database were used to evaluate the correlation between Ly6E expression levels and cancer patient survival. After analyzing Ly6E expression levels in human breast cancer tissues and tumor cell lines, we generated Ly6E knockout (KO) and overexpression (OE) mouse cell lines. Cell proliferation ability in vitro and the ability of growth and metastasis in mouse tumor models were compared between KO/OE and wild-type tumor cells. On day 7 after tumor implantation, tumor tissues were separated for flow cytometric assay, bulk RNA sequencing and single-cell RNA sequencing (ScRNA-seq). The role of Ly6E-expressing tumor cell on macrophage was analyzed in vitro.
resultsOur result surprisingly found that high Ly6E expression levels were associated with CD8
conclusionOur study illuminated that Ly6E-expressing tumor cells facilitated the accumulation of M2 macrophages in TME, which contributes to CD8
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