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Objective <p> To investigate the impact of neoadjuvant hormonal therapy (NHT) on interleukin‑17&#xa0;A (IL‑17&#xa0;A) signaling and inflammation in prostate cancer (PCa), and to explore the role of the IL‑17&#xa0;A/signal transducer and activator of transcription 3 (STAT3) axis in tumor progression after androgen deprivation.</p> Methods <p> Paired prostate tissue samples from 27 patients receiving ≥ 3 months of NHT were analyzed. Histological inflammation was assessed by hematoxylin-eosin staining. Immunohistochemistry was used to evaluate IL-17&#xa0;A, interleukin‑17 receptor A (IL‑17RA), interleukin‑17 receptor C (IL‑17RC), STAT3, and androgen receptor (AR). Statistical analyses were performed to examine differences in expression and correlations between markers.</p> Results <p> Chronic inflammation significantly increased in tumor tissues after NHT (<i>P</i> &lt; 0.05). IL-17&#xa0;A and IL-17RC expression were higher in tumor tissues than adjacent benign tissues (<i>P</i> &lt; 0.001), with further upregulation after NHT (<i>P</i> &lt; 0.05). Longer NHT duration (≥ 6 months) was associated with elevated IL-17&#xa0;A and IL-17RC levels. IL-17&#xa0;A expression positively correlated with STAT3 (<i>r</i> = 0.388, <i>P</i> = 0.045), but not with androgen receptor (AR).</p> Conclusions <p> Prolonged NHT enhances IL-17&#xa0;A/IL-17RC-mediated inflammation in prostate cancer, potentially promoting tumor progression through STAT3 activation. Targeting the IL-17&#xa0;A/STAT3 axis may offer therapeutic potential for advanced prostate cancer, although further validation is required before NHT can be incorporated into clinical guidelines.</p>

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Prolonged neoadjuvant hormonal therapy enhances IL-17 A/STAT3-mediated inflammation in prostate cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月14日

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  • Yirui Wei,
  • Yifan Chu,
  • Siqi Wang,
  • Dawei Xie,
  • Hao Wang,
  • Weifeng He,
  • Pushen Yang,
  • Jianwen Wang

摘要

Objective

To investigate the impact of neoadjuvant hormonal therapy (NHT) on interleukin‑17 A (IL‑17 A) signaling and inflammation in prostate cancer (PCa), and to explore the role of the IL‑17 A/signal transducer and activator of transcription 3 (STAT3) axis in tumor progression after androgen deprivation.

Methods

Paired prostate tissue samples from 27 patients receiving ≥ 3 months of NHT were analyzed. Histological inflammation was assessed by hematoxylin-eosin staining. Immunohistochemistry was used to evaluate IL-17 A, interleukin‑17 receptor A (IL‑17RA), interleukin‑17 receptor C (IL‑17RC), STAT3, and androgen receptor (AR). Statistical analyses were performed to examine differences in expression and correlations between markers.

Results

Chronic inflammation significantly increased in tumor tissues after NHT (P < 0.05). IL-17 A and IL-17RC expression were higher in tumor tissues than adjacent benign tissues (P < 0.001), with further upregulation after NHT (P < 0.05). Longer NHT duration (≥ 6 months) was associated with elevated IL-17 A and IL-17RC levels. IL-17 A expression positively correlated with STAT3 (r = 0.388, P = 0.045), but not with androgen receptor (AR).

Conclusions

Prolonged NHT enhances IL-17 A/IL-17RC-mediated inflammation in prostate cancer, potentially promoting tumor progression through STAT3 activation. Targeting the IL-17 A/STAT3 axis may offer therapeutic potential for advanced prostate cancer, although further validation is required before NHT can be incorporated into clinical guidelines.