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Background <p>A close relationship exists between castration-resistant prostate cancer (CRPC) and histidine metabolism by gut microbes. However, the effects of the histidine metabolite imidazole propionate (IMP) on prostate cancer (PCa) and its underlying mechanisms are not well understood.</p> Methods <p>We first assessed the effects of IMP on cell proliferation and migration at the cellular level. Subsequently, we investigated the mechanism of action of IMP using transcriptome sequencing, qPCR, and Western blot analysis. Finally, we validated our findings in vivo using a mouse model.</p> Results <p>Histidine had no effect on PCa cell proliferation; however, IMP significantly inhibited the proliferation and migration of PC3 and DU145 cells. Mechanistic studies indicate that IMP exerts its effects by upregulating PDZK1 expression, which subsequently inhibits the phosphorylation of the PI3K-AKT pathway.</p> Conclusions <p>In conclusion, IMP significantly inhibits the progression of PCa, offering new insights into potential treatments for CRPC.</p>

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Microbially produced imidazole propionate impairs prostate cancer progression through PDZK1

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年1月16日

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  • Shengkai Jin,
  • Yuhua Zhou,
  • Jing Lv,
  • Yichen Lu,
  • Yuwei Zhang,
  • Menglu Li,
  • Ninghan Feng

摘要

Background

A close relationship exists between castration-resistant prostate cancer (CRPC) and histidine metabolism by gut microbes. However, the effects of the histidine metabolite imidazole propionate (IMP) on prostate cancer (PCa) and its underlying mechanisms are not well understood.

Methods

We first assessed the effects of IMP on cell proliferation and migration at the cellular level. Subsequently, we investigated the mechanism of action of IMP using transcriptome sequencing, qPCR, and Western blot analysis. Finally, we validated our findings in vivo using a mouse model.

Results

Histidine had no effect on PCa cell proliferation; however, IMP significantly inhibited the proliferation and migration of PC3 and DU145 cells. Mechanistic studies indicate that IMP exerts its effects by upregulating PDZK1 expression, which subsequently inhibits the phosphorylation of the PI3K-AKT pathway.

Conclusions

In conclusion, IMP significantly inhibits the progression of PCa, offering new insights into potential treatments for CRPC.