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Purpose <p>Indole-3-carbinol (I3C) is shown to possess multiple pharmacological activities such as anti-inflammatory, antimicrobial, antioxidant, antiviral, and anti-cancer activities. It is widely accepted as modulator of multiple signaling pathways particularly those related to cell cycle, cell growth and division, angiogenesis, apoptosis and immunity.&#xa0;We explored the metabolic reprogramming based on&#xa0;treatment with&#xa0;I3C in mice prostate tissue.</p> Methods <p>In this study we utilized Pten knockout (KO)-induced prostate tumorigenesis mouse model to examine mechanism of action of I3C via metabolic rewiring. Phosphatase and tensin homolog deleted on chromosome 10 (Pten), a tumor suppressor gene is frequently found to be mutated or deleted in prostate cancer. Untargeted metabolomics was performed using liquid-chromatography mass-spectrometry (LC–MS) based platform to investigate Pten-dependent and Pten-independent metabolic targets of I3C.</p> Results <p>The most impacted pathways by I3C included pyrimidine metabolism, arginine and proline metabolism, porphyrin metabolism, citrate cycle and lipoic acid metabolism.</p> Conclusion <p>These pathways taken together help in understanding the overall health beneficial effects of I3C.</p>

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Dietary phytochemical indole-3-carbinol regulates metabolic reprogramming in mouse prostate tissue

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月4日

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  • Rebecca Mary Peter,
  • Md. Shahid Sarwar,
  • Lujing Wang,
  • Pochung Chou,
  • Chao Wang,
  • Yujue Wang,
  • Xiaoyang Su,
  • Ah-Ng Kong

摘要

Purpose

Indole-3-carbinol (I3C) is shown to possess multiple pharmacological activities such as anti-inflammatory, antimicrobial, antioxidant, antiviral, and anti-cancer activities. It is widely accepted as modulator of multiple signaling pathways particularly those related to cell cycle, cell growth and division, angiogenesis, apoptosis and immunity. We explored the metabolic reprogramming based on treatment with I3C in mice prostate tissue.

Methods

In this study we utilized Pten knockout (KO)-induced prostate tumorigenesis mouse model to examine mechanism of action of I3C via metabolic rewiring. Phosphatase and tensin homolog deleted on chromosome 10 (Pten), a tumor suppressor gene is frequently found to be mutated or deleted in prostate cancer. Untargeted metabolomics was performed using liquid-chromatography mass-spectrometry (LC–MS) based platform to investigate Pten-dependent and Pten-independent metabolic targets of I3C.

Results

The most impacted pathways by I3C included pyrimidine metabolism, arginine and proline metabolism, porphyrin metabolism, citrate cycle and lipoic acid metabolism.

Conclusion

These pathways taken together help in understanding the overall health beneficial effects of I3C.