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CXCL1/IGHG1 signaling enhances crosstalk between tumor cells and tumor-associated macrophages to promote MC-LR-induced colorectal cancer progression

串扰 CXCL1型 癌症研究 肿瘤进展 肿瘤微环境 细胞生长 基因沉默 下调和上调 肿瘤细胞 化学 生物 癌症 免疫学 免疫系统 趋化因子 基因 生物化学 物理 光学 遗传学
作者
Lingqiao Wang,Weiyan Chen,Huidong Jin,Yao Tan,Chengwei Guo,Wenjuan Fu,Zhiling Wu,Ke Cui,Yiqi Wang,Zhiqun Qiu,Guowei Zhang,Wenbin Liu,Ziyuan Zhou
出处
期刊:Environmental Pollution [Elsevier]
卷期号:351: 124081-124081 被引量:1
标识
DOI:10.1016/j.envpol.2024.124081
摘要

Microcystin-leucine arginine (MC-LR) is a common cyantotoxin produced by hazardous cyanobacterial blooms, and eutrophication is increasing the contamination level of MC-LR in drinking water supplies and aquatic foods. MC-LR has been linked to colorectal cancer (CRC) progression associated with tumor microenvironment, however, the underlying mechanism is not clearly understood. In present study, by using GEO, KEGG, GESA and ImmPort database, MC-LR related differentially expressed genes (DEGs) and pathway- and gene set-enrichment analysis were performed. Of the three identified DEGs (CXCL1, GUCA2A and GDF15), CXCL1 was shown a positive association with tumor infiltration, and was validated to have a dominantly higher upregulation in MC-LR-treated tumor-associated macrophages (TAMs) rather than in MC-LR-treated CRC cells. Both CRC cell/macrophage co-culture and xenograft mouse models indicated that MC-LR stimulated TAMs to secrete CXCL1 resulting in promoted proliferation, migration, and invasion capability of CRC cells. Furtherly, IP-MS assay found that interaction between TAMs-derived CXCL1 and CRC cell-derived IGHG1 may enhance CRC cell proliferation and migration after MC-LR treatment, and this effect can be attenuated by silencing IGHG1 in CRC cell. In addition, molecular docking analysis, co-immunoprecipitation and immunofluorescence further proved the interactions between CXCL1 and IGHG1. In conclusion, CXCL1 secreted by TAMs can trigger IGHG1 expression in CRC cells, which provides a new clue in elucidating the mechanism of MC-LR-mediated CRC progression.
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