ArticleTranslational cancer research2025
MCRS1 is associated with immunosuppressive microenvironments in pan-cancer and promotes hepatocellular carcinoma malignant phenotypes.
Article in Translational cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Clinical outcomes and prognostic factors of systemic therapy combined with interventional treatment in hepatocellular carcinoma: a multicenter retrospective case series.Translational cancer research · 2026Article
- Regulation of immune tolerance in hepatocellular carcinoma by liver diseases: a review.Infectious agents and cancer · 2026Review
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4 authors.
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Abstract
Background: Pan-cancer analyses focused on the immunological significance and therapeutic potential of microspherule protein 1 (MCRS1) remain unreported. This study aims to define the pan-cancer immunological significance and therapeutic potential of MCRS1, with focused mechanistic dissection of its epigenetic-driven roles in hepatocellular carcinoma (HCC) progression. Methods: An integrated multi-omics approach was employed, encompassing bulk transcriptomics, single-cell RNA-sequencing (scRNA-seq), and functional validation. Data from public repositories including The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and the Human Protein Atlas (HPA) were analyzed using tools such as SangerBox, University of Alabama at Birmingham Cancer (UALCAN), Gene Expression Profiling Interactive Analysis (GEPIA), Kaplan-Meier plotter, and Tumor Immune Estimation Resource (TIMER). Expression patterns, prognostic significance, epigenetic regulation, interactions with immune infiltrates, and functional impact of MCRS1 on HCC malignant phenotypes were comprehensively assessed. Results: MCRS1 was upregulated in 24 malignancies (including HCC) and correlated with advanced stage, poor differentiation, and reduced survival (P<0.001). Hypomethylation of the MCRS1 promoter drove its overexpression in HCC, strongly associating with tumor progression. MCRS1 recruited M2-polarized macrophages (Rho =0.423, P=1.90e-16) and myeloid dendritic cells (Rho =0.560, P=7.87e-30). Spatial mapping confirmed MCRS1 Conclusions: Our pan-cancer analysis identifies MCRS1 as a key node linking epigenetic dysregulation and immunosuppression in HCC. Its promoter hypomethylation-driven overexpression is associated with an M2 macrophage-polarized, immune-resistant niche. These findings suggest that targeting MCRS1 may represent a strategy to overcome resistance to current immunotherapies.
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