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Results for “CD155”

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3 recordsLinked to original sources

PubMed2026

A TIGIT nanotrapping-guided STING-activatable immunometabolic strategy overcomes innate immune silence and T cell exhaustion in breast cancer.

Breast cancer exhibits a profoundly immunosuppressive tumor microenvironment (TME), where innate immune silence prevents antigen sensing and persistent T cell exhaustion limits effector responses, rendering most immunotherapies ineffective. Clinical profiling of 1093 The Cancer Genome Atlas (TCGA) cases identified a glucose-fueled glutathione (GSH)-glutathione peroxidase 4 (GPX4)-dihydrolipoamide S-acetyltransferase (DLAT) axis as a dominant metabolic shield that suppresses oxidative stress, and thereby enforces both stimulator of interferon genes (STING) silence and CD8+ T cell exclusion. To dismantle this barrier, we developed an immunometabolic nanotherapy, GOx/ES-CO-LDH@TIGIT-Nanotrap (TNT). In acidic tumors, proton-driven layered double hydroxide (LDH) disassembly releases glucose oxidase (GOx) and extremely small cuprous oxide (ES-CO). GOx depletes glucose and nicotinamide adenine dinucleotide phosphate (NADPH) to induce disulfidptosis, while ES-CO releases cuprous ions (Cu+) that trigger cuproptosis via binding to lipoylated mitochondrial proteins. Their mutual biochemical amplification produces a cycloacclerated disulfidptosis-cuproptosis cascade that collapses the GSH-GPX4-DLAT axis and restores STING activation. Meanwhile, the macrophage-derived T cell immunoreceptor with Ig and ITIM domains (TIGIT) Nanotrap sequesters CD155 to prevent T cell suppression. Together, this coordinated innate reactivation and adaptive rescue converts immune-cold tumors into STING-inflamed and T cell responsive lesions.

Female↗

PubMed2025

ZNF180 modulates tumor intrinsic immunotherapy resistance in melanoma through driving plasticity.

BACKGROUND: Based on our previous study, we have identified ZNF180, a zinc finger protein, as a pro-tumorigenic regulator in primary melanoma and a marker for poor prognosis. Herein, we report that ZNF180-regulated pathway, hence ZNF180-regulome, underlies resistance towards immune checkpoint inhibitions (ICIs). METHODS: To investigate regulatory roles of ZNF180 to confer these immune suppressive phenotypes, we performed ZNF180 knock-down in melanoma cells in vitro with different genetic backgrounds, namely A375 (BRAF-mutant) and SKMEL147 (NRAS-mutant) cells, and performed RNA- and ATAC-sequencing. We performed integrative analysis of RNA- and ATAC-sequencing data with publicly available sequencing data from ICI-treated cohorts to construct comprehensive model of ZNF180-regulome and its impacts on immune microenvironment. Further, we performed ZNF180 silencing in immune competent Yumm1.7 murine model to confirm the changes in immune microenvironments. RESULTS: ZNF180-regulome was predictive of ICI responses in independent bulk sequencing cohorts, and ZNF180+ tumors persisted after the therapy with immune-suppressive features such as MHC-I loss and CD155 expressions, the primary ligand to TIGIT inhibitory receptor. Further, ZNF180 silencing revealed its regulations on AP-1 transcription factors to drive melanoma reprogramming towards de-differentiated MITFlowAXLhigh cells, an established melanoma subtypes associated with recurrence and ICI resistance. In tandem, we observed that ZNF180+ tumor neighborhood significantly excluded with CD4 T-cells in metastatic tumor, and its silencing in immune competent murine model increased CD4 helper T-cell infiltrations with significant tumor regression in vivo. CONCLUSION: Collectively, these results indicate ZNF180 is a tumor intrinsic regulator of melanoma plasticity to drive de-differentiated phenotypes with immune-suppressive features including loss of immunogenicity, T-cell inhibitory signals through TIGIT/CD155 checkpoint and exclusion of CD4 helper T-cells. As ZNF180-regulome manifests in non-metastatic melanoma in contrast to the current focus of standard-of-care ICI on the metastatic disease, these results establish ZNF180-regulome as a biomarker and novel therapeutic avenue for early-stage, non-metastatic melanoma to intervene ICI resistance.

Immune checkpoint inhibition↗

PubMed2026

Transcriptomic Association Between Poliovirus Receptor (PVR/CD155) and Claudin Signaling Pathways in Colorectal Cancer.

BACKGROUND/AIM: Enterotoxigenic Bacteroides fragilis promotes colorectal carcinogenesis through toxin-mediated cleavage of E-cadherin, a process facilitated by membrane-associated Claudin-4 (CLDN4). Separately, the poliovirus receptor (PVR/CD155) modulates tumor epithelial and immune dynamics. This study explored potential transcriptomic interactions and co-expression frameworks between PVR and claudin signaling pathways in colorectal cancer. MATERIALS AND METHODS: Transcriptomic and proteomic data from the The Cancer Genome Atlas-colon adenocarcinoma cohort (TCGA-COAD) were evaluated. An exploratory E-cadherin Cleavage Index was modeled to capture transcript-protein discordance. To control for tissue composition heterogeneity without mathematical circularity, a de-circularized, non-parametric partial rank residual model adjusted for independent CLDN4 expression was deployed within the stable microsatellite-stable (MSS) sub-cohort (N=473). RESULTS: Multivariable survival models showed no independent associations between overall survival and continuous PVR (p=0.79) or CLDN3 (p=0.56) expression. Robust linear modeling revealed no significant baseline interaction between PVR and CLDN4 regarding the exploratory Cleavage Index (p=0.82). However, de-circularized partial correlation analysis revealed a highly stable, positive co-expression between PVR and CLDN3 (rho=0.2459, p=3.23×10-7). Both epithelial markers retained modest inverse correlations with the infiltrating lymphocytic axis (TIGIT and CD96). CONCLUSION: Baseline PVR expression is coordinated with CLDN3 tissue programs independent of general epithelial cellularity but does not interact with the CLDN4 axis or impact overall survival in an unexposed cohort. Because TCGA lacks virome or active microbial exposure tracking, these findings serve as baseline benchmarks for future context-dependent mechanistic studies.

Bacteroides fragilis toxin↗