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趋化因子在肺癌进展中的新功能。

The novel functions of chemokines in lung cancer progression.

作者信息

Gong Xiaorui, Wang Xueying, Jin Jing, Gong Zhiqiang

机构信息

Medical Oncology Department of Thoracic Cancer (II), Cancer Hospital of China Medical University Liaoning Cancer Hospital and Institute, Cancer Hospital of Dalian University of Technology, Shenyang, China.

Department of Child Healthcare, Shenyang Children's Hospital, Shenyang, China.

出版信息

Front Immunol. 2025 Jun 18;16:1607225. doi: 10.3389/fimmu.2025.1607225. eCollection 2025.

DOI:10.3389/fimmu.2025.1607225
PMID:40607416
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12213639/
Abstract

Chemokines are key molecules that regulate immune cell migration and play critical roles in the tumor microenvironment. In lung cancer, chemokine dysregulation is closely linked to tumor progression. They promote immune cell infiltration and interact with tumor cells, enhancing tumor invasiveness and metastatic potential. This review highlights chemokine-mediated mechanisms, focusing on CCR9/CCL25 and CXCL12/CXCR4 axes, which promote tumor growth, metastasis, and immune evasion via PI3K/AKT and MAPK signaling. Elevated expression of these pathways correlates with poor outcomes and aggressive phenotypes. In SCLC, CXCR4 inhibitors show therapeutic promise when combined with chemotherapy or immunotherapy. This review summarizes the prognostic and therapeutic relevance of chemokines in lung cancer progression.

摘要

趋化因子是调节免疫细胞迁移的关键分子,在肿瘤微环境中发挥着至关重要的作用。在肺癌中,趋化因子失调与肿瘤进展密切相关。它们促进免疫细胞浸润并与肿瘤细胞相互作用,增强肿瘤的侵袭性和转移潜能。本综述重点介绍趋化因子介导的机制,着重于CCR9/CCL25和CXCL12/CXCR4轴,它们通过PI3K/AKT和MAPK信号通路促进肿瘤生长、转移和免疫逃逸。这些通路的高表达与不良预后和侵袭性表型相关。在小细胞肺癌中,CXCR4抑制剂与化疗或免疫疗法联合使用时显示出治疗前景。本综述总结了趋化因子在肺癌进展中的预后和治疗相关性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9582/12213639/8dd841c93c0d/fimmu-16-1607225-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9582/12213639/8dd841c93c0d/fimmu-16-1607225-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9582/12213639/8dd841c93c0d/fimmu-16-1607225-g001.jpg

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本文引用的文献

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ST6GalNAc-I regulates tumor cell sialylation via NECTIN2/MUC5AC-mediated immunosuppression and angiogenesis in non-small cell lung cancer.ST6GalNAc-I通过NECTIN2/MUC5AC介导的免疫抑制和血管生成调节非小细胞肺癌中的肿瘤细胞唾液酸化。
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Tumor cell-intrinsic BIN1 deficiency promotes the immunosuppression and impedes ferroptosis of non-small cell lung cancer via G3BP1-mediated degradation of STAT1.肿瘤细胞内在的BIN1缺陷通过G3BP1介导的STAT1降解促进非小细胞肺癌的免疫抑制并阻碍铁死亡。
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Therapeutic efficacy of TMTP1-modified EVs in overcoming bone metastasis and immune resistance in PIK3CA mutant NSCLC.
TMTP1修饰的细胞外囊泡在克服PIK3CA突变型非小细胞肺癌骨转移和免疫抵抗方面的治疗效果
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p53 transcriptionally activates DCP1B to suppress tumor progression and enhance tumor sensitivity to PI3K blockade in non-small cell lung cancer.p53通过转录激活DCP1B来抑制非小细胞肺癌的肿瘤进展并增强肿瘤对PI3K阻断的敏感性。
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Selective Depletion of CCR8+Treg Cells Enhances the Antitumor Immunity of Cytotoxic T Cells in Lung Cancer by Dendritic Cells.CCR8+调节性T细胞的选择性消耗通过树突状细胞增强肺癌中细胞毒性T细胞的抗肿瘤免疫。
J Thorac Oncol. 2025 Mar 6. doi: 10.1016/j.jtho.2025.02.029.
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