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<p>Solasonine (SS), a natural steroidal alkaloid, exhibits potential antitumor activity. However, its effects on non-small cell lung cancer (NSCLC) and the mechanisms remain incompletely explored. The inhibitory effects of SS on malignant behaviors of NSCLC cells (A549 and H157) were assessed utilizing CCK-8, EdU, TUNEL, wound healing, and Transwell assays. In addition, PD-L1 overexpression (oe-PD-L1) was performed to evaluate its functional role and to conduct rescue experiments. Its antitumor efficacy in vivo was validated in subcutaneous xenograft models. Western blotting, immunofluorescence, and immunohistochemistry were employed to analyze the STAT3/PD-L1 pathway and epithelial-mesenchymal transition (EMT)-relevant markers. SS significantly suppressed proliferation, induced apoptosis, and inhibited migration and invasion of NSCLC cells. Mechanistically, SS attenuated interleukin-6-induced STAT3/PD-L1 signaling activation and reversed the EMT process, as evidenced by E-cadherin upregulation and N-cadherin downregulation. Notably, PD-L1 overexpression partially reversed the inhibitory effects of SS on NSCLC cells. In vivo, SS administration markedly inhibited tumor growth and reversed EMT. Furthermore, it reduced the p-STAT3/STAT3 ratio and decreased PD-L1 and c-Myc expression in tumor tissues. SS exerts potent anti-NSCLC effects by blocking the STAT3/PD-L1 signaling pathway and suppressing EMT, suggesting its potential as a therapeutic agent for NSCLC.</p>

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Solasonine suppresses non-small cell lung cancer progression by inhibiting the STAT3/PD-L1 axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月2日

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  • Ling Zheng,
  • Qiankun Song,
  • Junyan Liang

摘要

Solasonine (SS), a natural steroidal alkaloid, exhibits potential antitumor activity. However, its effects on non-small cell lung cancer (NSCLC) and the mechanisms remain incompletely explored. The inhibitory effects of SS on malignant behaviors of NSCLC cells (A549 and H157) were assessed utilizing CCK-8, EdU, TUNEL, wound healing, and Transwell assays. In addition, PD-L1 overexpression (oe-PD-L1) was performed to evaluate its functional role and to conduct rescue experiments. Its antitumor efficacy in vivo was validated in subcutaneous xenograft models. Western blotting, immunofluorescence, and immunohistochemistry were employed to analyze the STAT3/PD-L1 pathway and epithelial-mesenchymal transition (EMT)-relevant markers. SS significantly suppressed proliferation, induced apoptosis, and inhibited migration and invasion of NSCLC cells. Mechanistically, SS attenuated interleukin-6-induced STAT3/PD-L1 signaling activation and reversed the EMT process, as evidenced by E-cadherin upregulation and N-cadherin downregulation. Notably, PD-L1 overexpression partially reversed the inhibitory effects of SS on NSCLC cells. In vivo, SS administration markedly inhibited tumor growth and reversed EMT. Furthermore, it reduced the p-STAT3/STAT3 ratio and decreased PD-L1 and c-Myc expression in tumor tissues. SS exerts potent anti-NSCLC effects by blocking the STAT3/PD-L1 signaling pathway and suppressing EMT, suggesting its potential as a therapeutic agent for NSCLC.