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<p>It has been reported that anlotinib exhibits antitumor efficacy in various cancers. However, the potential mechanisms by which anlotinib affects the immunosuppressive characteristics observed in tumor angiogenesis have not been fully elucidated. Therefore, we aimed to determine the potential of anlotinib in improving the effectiveness of PD-1/PD-L1 blockade therapy in lung cancer. An LLC mouse model was established by xenograft tumor model to evaluate the synergistic effects of anlotinib and anti-PD-1. Furthermore, changes in tumor vascular structure and T-cell infiltration were assessed using immunohistochemistry and flow cytometry. Clinical information from 198 lung cancer patients was collected to further analyze the relationship between Ki67 expression and patient survival as well as the synergistic effects. The study demonstrated that anlotinib successfully inhibited LLC cell growth. Additionally, anlotinib reduced related protein expressions in JAK2/STAT3 pathway. Mice in the anlotinib group exhibited lower expression levels of PD-L1 and VEGF-A and decreased intratumoral microvascular density. Moreover, PD-1/PD-L1 blockade combined with anlotinib promoted CD4 + T-cell infiltration into tumors, ultimately enhancing antitumor activity. Clinically, lung cancer patients treated with anlotinib and anti-PD-1 showed reduced Ki67 expression and improved survival rates. In conclusion, anlotinib improves tumor vascular structure and CD4 + T-cell infiltration by downregulating JAK2/STAT3 signaling, thereby enhancing the efficacy of PD-1 blockade in lung cancer.</p>

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Anlotinib promotes CD4 + T cell infiltration and enhances the anti-tumor effect of PD-1 blockade in lung cancer

  • 期刊论文

  • 发表日期：

    2025年10月13日

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  • Mengyan Zhang,
  • Lingyun Liu,
  • Hongying Zheng,
  • Mingqiu Chen,
  • Jiancheng Li

摘要

It has been reported that anlotinib exhibits antitumor efficacy in various cancers. However, the potential mechanisms by which anlotinib affects the immunosuppressive characteristics observed in tumor angiogenesis have not been fully elucidated. Therefore, we aimed to determine the potential of anlotinib in improving the effectiveness of PD-1/PD-L1 blockade therapy in lung cancer. An LLC mouse model was established by xenograft tumor model to evaluate the synergistic effects of anlotinib and anti-PD-1. Furthermore, changes in tumor vascular structure and T-cell infiltration were assessed using immunohistochemistry and flow cytometry. Clinical information from 198 lung cancer patients was collected to further analyze the relationship between Ki67 expression and patient survival as well as the synergistic effects. The study demonstrated that anlotinib successfully inhibited LLC cell growth. Additionally, anlotinib reduced related protein expressions in JAK2/STAT3 pathway. Mice in the anlotinib group exhibited lower expression levels of PD-L1 and VEGF-A and decreased intratumoral microvascular density. Moreover, PD-1/PD-L1 blockade combined with anlotinib promoted CD4 + T-cell infiltration into tumors, ultimately enhancing antitumor activity. Clinically, lung cancer patients treated with anlotinib and anti-PD-1 showed reduced Ki67 expression and improved survival rates. In conclusion, anlotinib improves tumor vascular structure and CD4 + T-cell infiltration by downregulating JAK2/STAT3 signaling, thereby enhancing the efficacy of PD-1 blockade in lung cancer.