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<p>Renal cell carcinoma (RCC) remains a clinically challenging malignancy because of its marked molecular heterogeneity and the limited long-term efficacy of current systemic therapies. Albiflorin, a major bioactive constituent of <i>Paeonia lactiflora</i>, has been reported to possess anti-inflammatory, antioxidant, and cytoprotective activities, whereas its potential role in RCC remains unclear. In the present study, the anti-RCC activity of albiflorin was investigated by integrating in vitro experiments, network pharmacology, and molecular docking, and experimental validation. CCK-8 assays showed that albiflorin reduced the viability of 786-O and A498 cells in a concentration-dependent manner, with lower IC50 values in RCC cells than in HK-2 cells. EdU incorporation and wound-healing assays further demonstrated that albiflorin suppressed RCC cell proliferation and migration. Albiflorin-related targets were collected from SuperPred and SwissTargetPrediction, while RCC-related targets were obtained from the KICH, KIRC, and KIRP datasets in TCGA. Sixty-four overlapping targets were identified. GO and KEGG enrichment analyses indicated that these targets were mainly associated with signal transduction, apoptosis, migration, angiogenesis, and cancer-related pathways, including MAPK, PI3K-Akt, Ras, and calcium signaling. Candidate target screening identified EGFR, MMP9, and FGF2 as representative candidate targets. Molecular docking supported the potential binding of albiflorin to EGFR and MMP9. RT-qPCR showed that albiflorin reduced <i>MMP9</i> and <i>FGF2</i> mRNA expression, whereas <i>EGFR</i> mRNA was not markedly altered. Western blotting showed decreased EGFR and ERK phosphorylation, and EGF stimulation partially restored EGFR/MAPK signaling activation in albiflorin-treated RCC cells. These findings suggest that albiflorin inhibits RCC cell viability, proliferation, and migration, partly through suppression of EGFR/MAPK signaling and regulation of tumor progression-related molecules.</p>

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Integrated experimental and network pharmacology analyses reveal inhibitory effects of albiflorin on renal cell carcinoma cells

  • 期刊论文

  • 发表日期：

    2026年5月27日

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  • Kai Meng,
  • Yu Zhang,
  • Lu Ma,
  • Zixuan Chen,
  • Haining Qian,
  • Zongrun Sun,
  • Xing Jia,
  • Min Liu

摘要

Renal cell carcinoma (RCC) remains a clinically challenging malignancy because of its marked molecular heterogeneity and the limited long-term efficacy of current systemic therapies. Albiflorin, a major bioactive constituent of Paeonia lactiflora, has been reported to possess anti-inflammatory, antioxidant, and cytoprotective activities, whereas its potential role in RCC remains unclear. In the present study, the anti-RCC activity of albiflorin was investigated by integrating in vitro experiments, network pharmacology, and molecular docking, and experimental validation. CCK-8 assays showed that albiflorin reduced the viability of 786-O and A498 cells in a concentration-dependent manner, with lower IC50 values in RCC cells than in HK-2 cells. EdU incorporation and wound-healing assays further demonstrated that albiflorin suppressed RCC cell proliferation and migration. Albiflorin-related targets were collected from SuperPred and SwissTargetPrediction, while RCC-related targets were obtained from the KICH, KIRC, and KIRP datasets in TCGA. Sixty-four overlapping targets were identified. GO and KEGG enrichment analyses indicated that these targets were mainly associated with signal transduction, apoptosis, migration, angiogenesis, and cancer-related pathways, including MAPK, PI3K-Akt, Ras, and calcium signaling. Candidate target screening identified EGFR, MMP9, and FGF2 as representative candidate targets. Molecular docking supported the potential binding of albiflorin to EGFR and MMP9. RT-qPCR showed that albiflorin reduced MMP9 and FGF2 mRNA expression, whereas EGFR mRNA was not markedly altered. Western blotting showed decreased EGFR and ERK phosphorylation, and EGF stimulation partially restored EGFR/MAPK signaling activation in albiflorin-treated RCC cells. These findings suggest that albiflorin inhibits RCC cell viability, proliferation, and migration, partly through suppression of EGFR/MAPK signaling and regulation of tumor progression-related molecules.