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<p>This study involves the evaluation of the Fei Jin Sheng formula (FJS), a well-established traditional Chinese medicine (TCM) treatment for non-small cell lung cancer (NSCLC), aiming to address the heightened mortality rates associated with this form of lung cancer. By examining its multi-targeted routes and activities in vivo, we hope to clarify its complex molecular mechanisms. Liquid chromatography-tandem mass spectrometry and network pharmacology were used to identify FJS components and targets. Using organ histology and bi-weekly weight assessments of tumors and bodies and Lewis tumor model tumors, FJS efficacy and safety were assessed, while immunohistochemistry of tumor tissues was used to elucidate anti-tumor mechanisms. Based on research that had been previously conducted, FJS controls over 30 pathways and targets 15 critical proteins, including the <i>MAPK</i> pathway, in treating NSCLC. In vivo studies demonstrate that FJS reduces tumor proliferation by decreasing expression of <i>ERK1/2</i>, <i>p-ERK1/2</i>, <i>MEK1/2</i>, and <i>p-MEK1/2</i>, without affecting the structure of the liver, spleen, or kidney in mice. FJS is non-toxic and has the potential to treat NSCLC in vivo by inhibiting the <i>MAPK</i> signaling pathway.</p>

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Experimental investigation and network pharmacology-based analysis of the anticancer mechanisms of Fei Jin Sheng formula

  • 期刊论文

  • 发表日期：

    2026年7月16日

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  • Zhen Yan,
  • Qian Li,
  • Jian-Xiang Chen,
  • Ying-Gen Sheng,
  • Tian Xie

摘要

This study involves the evaluation of the Fei Jin Sheng formula (FJS), a well-established traditional Chinese medicine (TCM) treatment for non-small cell lung cancer (NSCLC), aiming to address the heightened mortality rates associated with this form of lung cancer. By examining its multi-targeted routes and activities in vivo, we hope to clarify its complex molecular mechanisms. Liquid chromatography-tandem mass spectrometry and network pharmacology were used to identify FJS components and targets. Using organ histology and bi-weekly weight assessments of tumors and bodies and Lewis tumor model tumors, FJS efficacy and safety were assessed, while immunohistochemistry of tumor tissues was used to elucidate anti-tumor mechanisms. Based on research that had been previously conducted, FJS controls over 30 pathways and targets 15 critical proteins, including the MAPK pathway, in treating NSCLC. In vivo studies demonstrate that FJS reduces tumor proliferation by decreasing expression of ERK1/2, p-ERK1/2, MEK1/2, and p-MEK1/2, without affecting the structure of the liver, spleen, or kidney in mice. FJS is non-toxic and has the potential to treat NSCLC in vivo by inhibiting the MAPK signaling pathway.