结直肠癌 (CRC) 涉及肿瘤细胞和免疫细胞（特别是单核细胞）之间复杂的相互作用，从而导致免疫抑制。本研究利用 THP-1 细胞和 CRC 细胞系的体外共培养系统探索了这些相互作用，采用定量蛋白质组学来分析单核细胞中的蛋白质变化。利用多种分析方法来描绘改变的蛋白质组景观，识别关键蛋白质及其相关的功能途径，以进行全面的数据分析。通过与公开的 TCGA 和 GEO 数据集交叉引用来选择和验证差异表达蛋白 (DEP)，以探索其潜在的临床意义。我们的分析确定了 161 个上调 DEP 和 130 个下调 DEP。富集结果显示单核细胞的粘附和先天免疫功能受损，可能促进癌症进展。 FN1、THSB1 和 JUN 的下调可能会导致这些损伤。此外，ADAMTSL4、PRAM1、GPNMB 和 NPC2 在单核细胞上的过度表达与 CRC 患者的不良预后结果相关，这表明潜在的生物标志物或治疗靶点。这项研究阐明了单核细胞响应 CRC 细胞的蛋白质组图谱，为未来研究肿瘤微环境中癌细胞和单核细胞之间的串扰提供了线索。

Colorectal cancer (CRC) involves a complex interaction between tumor cells and immune cells, notably monocytes, leading to immunosuppression. This study explored these interactions using in vitro coculture systems of THP-1 cells and CRC cell lines, employing quantitative proteomics to analyze protein changes in monocytes. Multiple analytical methods were utilized to delineate the altered proteomic landscape, identify key proteins, and their associated functional pathways for comprehensive data analysis. Differentially expressed proteins (DEPs) were selected and validated by cross-referencing them with publicly available TCGA and GEO data sets to explore their potential clinical significance. Our analysis identified 161 up-regulated and 130 down-regulated DEPs. The enrichment results revealed impairments in adhesion and innate immune functions in monocytes, potentially facilitating cancer progression. The down-regulation of FN1, THSB1, and JUN may contribute to these impairments. Furthermore, the overexpression of ADAMTSL4, PRAM1, GPNMB, and NPC2 on monocytes was associated with unfavorable prognostic outcomes in CRC patients, suggesting potential biomarkers or therapeutic targets. This study illustrated the proteomic landscape of monocytes in response to CRC cells, providing clues for future investigations of the crosstalk between cancer cells and monocytes within the tumor microenvironment.