ArticleBMC cancer2026
Ethyl caffeate reprograms tumor-associated macrophages to enhance CD8
Article in BMC cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
backgroundThe colorectal cancer (CRC) tumor microenvironment contains diverse myeloid populations that critically regulate antitumor immunity and therapeutic response. Tumor-associated macrophages are key regulators of macrophage-T-cell crosstalk within the CRC microenvironment. This study aimed to investigate the antitumor effects of Ethyl caffeate (EC) and determine whether EC modulates macrophage-associated immune remodeling in CRC.
methodsPublic single-cell RNA sequencing data from CRC tissues were analyzed to characterize myeloid infiltration, macrophage heterogeneity, Cell-cell communication, pseudotime trajectories, and macrophage-associated prognostic signatures. RAW264.7 cells and bone marrow-derived macrophages (BMDMs) were used to evaluate the effects of EC on macrophage viability and polarization in vitro. An immunogenic syngeneic MC38 CRC model was established in C57BL/6 mice to assess the antitumor activity of EC. Flow cytometry was used to quantify tumor infiltrating macrophages, CD86⁺ M1-like macrophages, CD8⁺ T cells, Granzyme B expression, and PD-1 expression. Clodronate liposome-mediated macrophage depletion was performed to determine whether the antitumor effect of EC was macrophage dependent.
resultsSingle-cell analysis revealed extensive myeloid infiltration and marked TAM heterogeneity in CRC. State-specific analyses identified CXCL9/CXCL10 IFN-responsive TAMs as a transitional immune activating population closely associated with CXCL10-CD8
conclusionsEC suppresses colorectal tumor growth at least partly through macrophage-dependent immune remodeling. These findings identify EC as a potential macrophage-reprogramming compound that enhances CD8⁺ T-cell antitumor immunity in CRC.
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