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Purpose <p>Benign prostatic hyperplasia (BPH) is a leading cause of voiding symptoms in aging men. Telomerase reverse transcriptase (TERT), a key regulator of cellular senescence and tissue remodeling, has not been systematically examined in human voiding symptoms, though genome-wide association studies suggested a role in genetic and sporadic BPH.</p> Methods <p>Prostate tissues from patients undergoing laser enucleation for BPH were analyzed by RT-PCR. Clinical parameters were compared between TERT-positive and -negative patients. TERT expression in laser-enucleated tissues was tested for correlation with contractile smooth muscle receptors and the proliferation marker Ki67, and compared to tissues from radical prostatectomy for prostate cancer.</p> Results <p>In a cohort of 100 patients undergoing laser enucleation of the prostate, we detected prostatic TERT mRNA in 81% of samples. Patients with TERT-positive tissues displayed clinically relevant higher symptom scores (22.5 vs. 17.4, <i>p</i> = 0.0407), and more pronounced post-void residual urine (80 vs. 142&#xa0;ml). Prostate volume and free PSA showed no relationship with TERT expression. TERT expression correlated with expression of α<sub>1A</sub>-adrenoceptors (<i>p</i> &lt; 0.0001), endothelin receptor A (<i>p</i> &lt; 0.0001) and B (<i>p</i> &lt; 0.0001), thromboxane receptor (<i>p</i> &lt; 0.0001), thromboxane synthase (<i>p</i> = 0.0050) and Ki67 (<i>p</i> = 0.0181). TERT expression was 460-fold higher (<i>p</i> = 0.0015) in laser-enucleated than in periurethral prostatectomized tissues.</p> Conclusions <p>TERT expression associates with higher symptom severity in laser-enucleated BPH patients, and correlates with targets imparting drug resistance. We propose that TERT acts as a molecular switch, marking a clinically more severe BPH phenotype. This finding raises the possibility of targeted intervention in BPH patients with TERT-driven pathology.</p>

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TERT expression in human prostate tissue reveals a potential molecular switch in benign prostatic hyperplasia progression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月11日

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  • Yajie Xu,
  • Sheng Hu,
  • Laurenz Berger,
  • Philip Nicola,
  • Philipp Weinhold,
  • Alexander Tamalunas,
  • Christian G. Stief,
  • Martin Hennenberg,
  • Patrick Keller

摘要

Purpose

Benign prostatic hyperplasia (BPH) is a leading cause of voiding symptoms in aging men. Telomerase reverse transcriptase (TERT), a key regulator of cellular senescence and tissue remodeling, has not been systematically examined in human voiding symptoms, though genome-wide association studies suggested a role in genetic and sporadic BPH.

Methods

Prostate tissues from patients undergoing laser enucleation for BPH were analyzed by RT-PCR. Clinical parameters were compared between TERT-positive and -negative patients. TERT expression in laser-enucleated tissues was tested for correlation with contractile smooth muscle receptors and the proliferation marker Ki67, and compared to tissues from radical prostatectomy for prostate cancer.

Results

In a cohort of 100 patients undergoing laser enucleation of the prostate, we detected prostatic TERT mRNA in 81% of samples. Patients with TERT-positive tissues displayed clinically relevant higher symptom scores (22.5 vs. 17.4, p = 0.0407), and more pronounced post-void residual urine (80 vs. 142 ml). Prostate volume and free PSA showed no relationship with TERT expression. TERT expression correlated with expression of α1A-adrenoceptors (p < 0.0001), endothelin receptor A (p < 0.0001) and B (p < 0.0001), thromboxane receptor (p < 0.0001), thromboxane synthase (p = 0.0050) and Ki67 (p = 0.0181). TERT expression was 460-fold higher (p = 0.0015) in laser-enucleated than in periurethral prostatectomized tissues.

Conclusions

TERT expression associates with higher symptom severity in laser-enucleated BPH patients, and correlates with targets imparting drug resistance. We propose that TERT acts as a molecular switch, marking a clinically more severe BPH phenotype. This finding raises the possibility of targeted intervention in BPH patients with TERT-driven pathology.