Transcriptional rewiring in cancer driven by POLR2A/RPB1: mechanistic insights, non-coding RNA crosstalk, and therapeutic opportunities

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Publicado en:Frontiers in Pharmacology vol. 16 (Dec 2025), p. 1745087-1745098
Autor principal: Szczepaniak, Adrian
Otros Autores: Jaskuła, Kinga, Zielińska, Marta, Godlewski, Jakub
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Frontiers Media SA
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Acceso en línea:Citation/Abstract
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100 1 |a Szczepaniak, Adrian  |u 1 Department of NeuroOncology, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland, 2 Doctoral School of Translational Medicine, Centre of Postgraduate Medical Education, Warsaw, Poland 
245 1 |a Transcriptional rewiring in cancer driven by POLR2A/RPB1: mechanistic insights, non-coding RNA crosstalk, and therapeutic opportunities 
260 |b Frontiers Media SA  |c Dec 2025 
513 |a Journal Article 
520 3 |a RNA polymerase II, together with its catalytic subunit RPB1 (encoded by POLR2A ), forms the core of the eukaryotic transcriptional machinery that drives the synthesis of protein-coding and regulatory RNA transcripts. Accumulating evidence indicates that dysregulation of POLR2A /RPB1 is a critical driver of oncogenesis, promoting uncontrolled proliferation, evasion of apoptosis, and extensive transcriptional reprogramming across multiple malignancies, frequently affected by recurrent 17p deletions co-occurring with major tumor suppressor loss events. Such coordinated genomic alterations create transcriptional dependency that may be exploited therapeutically. Beyond its canonical role in transcription, POLR2A /RPB1 operates within an extensive regulatory network involving non-coding RNAs. Notably, circular RNAs derived from the POLR2A transcript have emerged as stable post-transcriptional regulators that modulate tumorigenic signaling pathways. In these roles, circular POLR2A isoforms promote proliferation, migration, and therapy resistance in glioblastoma and clear-cell renal cell carcinoma by acting as miRNA sponges or by scaffolding protein complexes that activate pathways such as ERK. These findings suggest that disturbances in POLR2A function reshape not only transcriptional output but also the broader non-coding RNA landscape, thereby reinforcing malignant phenotypes. Moreover, pharmacological agents such as triptolide further highlight transcription-dependent vulnerabilities by destabilizing RPB1, offering promising therapeutic opportunities, particularly in drug-resistant cancers. Collectively, POLR2A /RPB1 emerges as a central node linking transcriptional control, noncoding RNA biogenesis, and oncogenic signaling, positioning it as a compelling candidate for biomarker development and targeted therapeutic intervention. 
653 |a Circular RNA 
653 |a Glioblastoma 
653 |a Tumor suppressor genes 
653 |a RNA polymerase 
653 |a Leukemia 
653 |a Nanoparticles 
653 |a miRNA 
653 |a Mutation 
653 |a Prostate cancer 
653 |a Drug resistance 
653 |a Phenotypes 
653 |a Isoforms 
653 |a MicroRNAs 
653 |a Tumorigenesis 
653 |a Post-transcription 
653 |a Non-coding RNA 
653 |a Localization 
653 |a Apoptosis 
653 |a Protein biosynthesis 
653 |a DNA-directed RNA polymerase 
653 |a Cell cycle 
653 |a Breast cancer 
653 |a Renal cell carcinoma 
653 |a Proteins 
653 |a Medical prognosis 
653 |a Biomarkers 
653 |a Phosphorylation 
653 |a Tumors 
653 |a Cell growth 
653 |a Malignancy 
653 |a Signal transduction 
653 |a Triptolide 
700 1 |a Jaskuła, Kinga  |u 3 Department of Experimental Genomics, Institute of Genetics and Animal Biotechnology, Polish Academy of Sciences, Jastrzębiec, Poland 
700 1 |a Zielińska, Marta  |u 4 Department of Biochemistry, Faculty of Medicine, Medical University of Lodz, Lodz, Poland 
700 1 |a Godlewski, Jakub  |u 1 Department of NeuroOncology, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland 
773 0 |t Frontiers in Pharmacology  |g vol. 16 (Dec 2025), p. 1745087-1745098 
786 0 |d ProQuest  |t Biological Science Database 
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