ArticleJournal of inflammation research2025
Comprehensive Analysis of Multi-Omics Data on RNA Polymerase as an Adverse Factor in Head and Neck Squamous Cell Carcinoma.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Alpha-like subunits of multisubunit RNA polymerases: insights into structure, function, and disease.RNA biology · 2026Review
- Microinflammation-Driven Gene Expression Dynamics in the Pathogenesis of Metabolic Disorders and Cancer.Biology · 2025Article
- Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: High transcription levels are essential for cancer cells to maintain their malignant phenotype. While RNA polymerases (POLRs) have been implicated in various transcriptional mechanisms, their impact on the tumor microenvironment (TME) remains poorly understood. Methods: We analyzed publicly available pan-cancer cohorts to evaluate the expression and genomic alterations of POLRs. Focusing on head and neck squamous cell carcinoma (HNSC), we integrated bulk RNA sequencing, single-cell, and spatial transcriptome data to identify POLR2C expression patterns and its potential regulation by Yin Yang 1 (YY1). In vitro and in vivo experiments were conducted to validate the functional role of the YY1-POLR2C axis in cancer proliferation and immune modulation. Results: POLRs were found to be aberrantly expressed in cancers and associated with genomic alterations. In HNSC, POLR up-regulation was linked to poor prognostic features. POLR2C was significantly up-regulated in malignant cells, and its expression appeared to be transcriptionally regulated by YY1. Functional studies demonstrated that the YY1-POLR2C axis drives cell-cycle dysregulation and malignant proliferation in HNSC. Additionally, high POLR expression negatively correlated with immune cell infiltration and facilitated immune evasion. Mechanistically, POLRs mediated frequent interactions between malignant and immune cells, potentially contributing to resistance to immunotherapy. Conclusion: This study highlights the dual role of POLRs in promoting malignant proliferation and shaping an immunosuppressive TME. POLR2C, regulated by YY1, emerges as a critical mediator in HNSC and a promising target for precision therapies.
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Registered trials
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