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<p>Prostate cancer (PCa) progression relies heavily on activation of the androgen signaling pathway, mediated by the androgen receptor (AR). Emerging evidence has shown that SND1 contributes to drug resistance and tumor growth of PCa. Therefore, this study aims to elucidate further the molecular mechanism by which SND1 promotes PCa progression through its post-transcriptional regulation of AR, intending to identify potential therapeutic targets for this disease. Our results revealed that SND1 and EIF3B were significantly elevated in PCa cells. Knockdown of either SND1 or EIF3B suppressed the PCa cell viability, proliferation, and migratory and invasive abilities of PCa cells. Mechanistically, SND1 directly bound to and enhanced the stability of EIF3B mRNA. Furthermore, EIF3B interacted with AR mRNA, thereby facilitating the translation process and AR protein levels. Notably, EIF3B overexpression counteracted the suppressive effects following SND1 knockdown on the aggressive characteristics of PCa cells. This study uncovers a novel SND1/EIF3B/AR regulatory axis in PCa, wherein SND1 stabilizes EIF3B mRNA, thereby enhancing AR translation and driving tumor progression. These findings highlight SND1 and EIF3B as promising prognostic biomarkers and potential therapeutic targets for advanced PCa.</p> Graphical abstract <p></p>

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SND1 regulates the androgen signaling axis by stabilizing EIF3B mRNA to facilitate the deterioration of prostate cancer

  • 期刊论文

  • 发表日期：

    2026年4月16日

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  • Ying Li,
  • Chengru Yang,
  • Guoli Cui,
  • Shiliang Gui,
  • Linlin Jia,
  • Yu Chen,
  • Honglin Niu,
  • Hua Xin

摘要

Prostate cancer (PCa) progression relies heavily on activation of the androgen signaling pathway, mediated by the androgen receptor (AR). Emerging evidence has shown that SND1 contributes to drug resistance and tumor growth of PCa. Therefore, this study aims to elucidate further the molecular mechanism by which SND1 promotes PCa progression through its post-transcriptional regulation of AR, intending to identify potential therapeutic targets for this disease. Our results revealed that SND1 and EIF3B were significantly elevated in PCa cells. Knockdown of either SND1 or EIF3B suppressed the PCa cell viability, proliferation, and migratory and invasive abilities of PCa cells. Mechanistically, SND1 directly bound to and enhanced the stability of EIF3B mRNA. Furthermore, EIF3B interacted with AR mRNA, thereby facilitating the translation process and AR protein levels. Notably, EIF3B overexpression counteracted the suppressive effects following SND1 knockdown on the aggressive characteristics of PCa cells. This study uncovers a novel SND1/EIF3B/AR regulatory axis in PCa, wherein SND1 stabilizes EIF3B mRNA, thereby enhancing AR translation and driving tumor progression. These findings highlight SND1 and EIF3B as promising prognostic biomarkers and potential therapeutic targets for advanced PCa.

Graphical abstract