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<p>The aim is to study the mechanism by which aloe emodin (AE) inhibits nasopharyngeal carcinoma (NPC) through regulating the epidermal growth factor receptor (EGFR)/SRC proto-oncogene (SRC)/signal transducer and activator of transcription 3 (STAT3) signaling pathway and programmed death-ligand 1 (<i>PD-L1</i>) expression. The methods are to predict AE target sites and NPC disease targets using a comprehensive database, construct protein interaction networks, and perform enrichment analysis and validate findings through molecular docking and in vitro experiments. Network pharmacology analysis identified 27 potential targets of AE acting on NPC, screening out 10 core targets including <i>EGFR</i>, <i>SRC</i>, and <i>STAT3</i>, which are closely associated with tumor signaling. KEGG enrichment analysis suggested AE may exert effects by regulating EGFR, mitogen-activated protein kinase (MAPK), and interleukin-17 (IL-17)-related pathways. Molecular docking revealed that AE exhibits strong binding activity against these core targets. In vitro validation showed that AE significantly suppressed the phosphorylation levels of EGFR, SRC, and STAT3, as well as PD-L1 expression, in NPC C666-1 and CNE1 cells, while reducing cell viability and migration capacity. Overexpression of STAT3 significantly attenuated AE’s inhibitory effects on cell proliferation and motility, further confirming STAT3 as a key target for AE’s mechanism of action. This study elucidates the multi-target mechanism of AE against NPC, with the EGFR/SRC/STAT3 axis identified as a critical downstream effector and its downstream PD-L1 expression, providing experimental evidence for its development as a natural antitumor drug.</p>

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Molecular mechanism of aloe emodin in combating nasopharyngeal carcinoma revealed through network pharmacology, molecular docking, and in vitro experiments

  • 期刊论文

  • 发表日期：

    2026年5月18日

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  • Zeng Xin,
  • Chunhong Li,
  • Mengqin Li,
  • Yuping Huang,
  • Jianhong Tang

摘要

The aim is to study the mechanism by which aloe emodin (AE) inhibits nasopharyngeal carcinoma (NPC) through regulating the epidermal growth factor receptor (EGFR)/SRC proto-oncogene (SRC)/signal transducer and activator of transcription 3 (STAT3) signaling pathway and programmed death-ligand 1 (PD-L1) expression. The methods are to predict AE target sites and NPC disease targets using a comprehensive database, construct protein interaction networks, and perform enrichment analysis and validate findings through molecular docking and in vitro experiments. Network pharmacology analysis identified 27 potential targets of AE acting on NPC, screening out 10 core targets including EGFR, SRC, and STAT3, which are closely associated with tumor signaling. KEGG enrichment analysis suggested AE may exert effects by regulating EGFR, mitogen-activated protein kinase (MAPK), and interleukin-17 (IL-17)-related pathways. Molecular docking revealed that AE exhibits strong binding activity against these core targets. In vitro validation showed that AE significantly suppressed the phosphorylation levels of EGFR, SRC, and STAT3, as well as PD-L1 expression, in NPC C666-1 and CNE1 cells, while reducing cell viability and migration capacity. Overexpression of STAT3 significantly attenuated AE’s inhibitory effects on cell proliferation and motility, further confirming STAT3 as a key target for AE’s mechanism of action. This study elucidates the multi-target mechanism of AE against NPC, with the EGFR/SRC/STAT3 axis identified as a critical downstream effector and its downstream PD-L1 expression, providing experimental evidence for its development as a natural antitumor drug.