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<p>Clear cell renal cell carcinoma (ccRCC) is a common and aggressive type of kidney cancer. This study aimed to investigate the effect of astragaloside IV (AS-IV) on ccRCC. A variety of cell experimental techniques were used, inducing macrophage polarization, and detecting relevant indicators by flow cytometry, qRT-PCR, immunofluorescence, MTT, wound healing, Transwell, and western blot. A nude mouse xenograft tumor model was constructed for in vivo studies, and siRNA interference technology was used to explore the signaling pathway. The results demonstrated successful macrophage polarization, with AS-IV inhibiting M2 macrophage polarization and promoting the transition from M0 to M1 polarization. Additionally, AS-IV suppressed ccRCC cell proliferation, migration, and invasion, while reversing the malignant effects of M2 macrophages. The study further revealed that AS-IV inhibited M2 polarization through the TLR4/NF-κB/STAT3 signaling pathway. In vivo experiments showed that AS-IV inhibited the growth of ccRCC tumors. This study revealed that AS-IV influences macrophage polarization by regulating the TLR4/NF-κB/STAT3 signaling pathway, thereby inhibiting the malignant phenotype of ccRCC. This finding provides new insights and potential therapeutic strategies for the treatment of ccRCC.</p>

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Astragaloside IV regulates macrophage polarization via the TLR4/NF-κB/STAT3 pathway to inhibit the malignant phenotype of renal clear cell carcinoma

  • 期刊论文

  • 发表日期：

    2025年5月9日

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  • Zhanshi Wang,
  • Chao Feng,
  • Guodong Chen,
  • Qi Cai

摘要

Clear cell renal cell carcinoma (ccRCC) is a common and aggressive type of kidney cancer. This study aimed to investigate the effect of astragaloside IV (AS-IV) on ccRCC. A variety of cell experimental techniques were used, inducing macrophage polarization, and detecting relevant indicators by flow cytometry, qRT-PCR, immunofluorescence, MTT, wound healing, Transwell, and western blot. A nude mouse xenograft tumor model was constructed for in vivo studies, and siRNA interference technology was used to explore the signaling pathway. The results demonstrated successful macrophage polarization, with AS-IV inhibiting M2 macrophage polarization and promoting the transition from M0 to M1 polarization. Additionally, AS-IV suppressed ccRCC cell proliferation, migration, and invasion, while reversing the malignant effects of M2 macrophages. The study further revealed that AS-IV inhibited M2 polarization through the TLR4/NF-κB/STAT3 signaling pathway. In vivo experiments showed that AS-IV inhibited the growth of ccRCC tumors. This study revealed that AS-IV influences macrophage polarization by regulating the TLR4/NF-κB/STAT3 signaling pathway, thereby inhibiting the malignant phenotype of ccRCC. This finding provides new insights and potential therapeutic strategies for the treatment of ccRCC.