Emodin Decreases Tumor-Associated Macrophages Accumulation and Suppresses Bladder Cancer Development by Inhibiting CXCL1 Secretion from Cancer-Associated Fibroblasts DOI
Fang Yu,

Nan Yu,

Lei Zhang

и другие.

Nutrition and Cancer, Год журнала: 2025, Номер unknown, С. 1 - 16

Опубликована: Март 20, 2025

Tumor-associated macrophages (TAMs) and cancer-associated fibroblasts (CAFs) are the most abundant stromal cells in bladder cancer (BC) microenvironment (TME). However, detailed mechanisms underlying TAM-CAF communication their contributions to BC progression remain incompletely understood. Emerging evidence shows that Emodin exerts anti-tumor effect on several tumor models by targeting TME. To date, impact of has not been previously reported. Our study firstly demonstrated significantly inhibited growth reduced TAM accumulation a murine model. markedly decreased serum levels multiple chemokines tumor-bearing mice, with CXCL1 showing pronounced reduction. Strikingly, selectively suppressed secretion CAFs but TAMs or cells. Furthermore, decrease migration induced was dependent CAF-derived CXCL1. Using subcutaneous model, we found failed inhibit when CXCL1-deficient were co-injected cells, underscoring critical role this process. Bioinformatics analysis further revealed elevated correlated negatively invasive/metastatic potential overall survival patients. In conclusion, our findings establish delays disrupting CXCL1-mediated crosstalk between TAMs.

Язык: Английский

Emodin Decreases Tumor-Associated Macrophages Accumulation and Suppresses Bladder Cancer Development by Inhibiting CXCL1 Secretion from Cancer-Associated Fibroblasts DOI
Fang Yu,

Nan Yu,

Lei Zhang

и другие.

Nutrition and Cancer, Год журнала: 2025, Номер unknown, С. 1 - 16

Опубликована: Март 20, 2025

Tumor-associated macrophages (TAMs) and cancer-associated fibroblasts (CAFs) are the most abundant stromal cells in bladder cancer (BC) microenvironment (TME). However, detailed mechanisms underlying TAM-CAF communication their contributions to BC progression remain incompletely understood. Emerging evidence shows that Emodin exerts anti-tumor effect on several tumor models by targeting TME. To date, impact of has not been previously reported. Our study firstly demonstrated significantly inhibited growth reduced TAM accumulation a murine model. markedly decreased serum levels multiple chemokines tumor-bearing mice, with CXCL1 showing pronounced reduction. Strikingly, selectively suppressed secretion CAFs but TAMs or cells. Furthermore, decrease migration induced was dependent CAF-derived CXCL1. Using subcutaneous model, we found failed inhibit when CXCL1-deficient were co-injected cells, underscoring critical role this process. Bioinformatics analysis further revealed elevated correlated negatively invasive/metastatic potential overall survival patients. In conclusion, our findings establish delays disrupting CXCL1-mediated crosstalk between TAMs.

Язык: Английский

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