ArticleJournal of Cancer2025
Unlocking ESCC Progression: CCL15-CCR1 Axis Activates AKT/ERK1/2/c-Jun/CDK2 Pathway.
Article in Journal of Cancer, 2025. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
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Abstract
Globally recognized as a major oncological concern, esophageal squamous cell carcinoma (ESCC) exhibits a high incidence rate among malignancies originating from the digestive system's epithelial lining. Tumor cells can secrete chemokine (C-C motif) ligand 15 (CCL15) to recruit C-C motif chemokine receptor 1 (CCR1)-positive macrophages, thereby facilitating immune evasion and promoting tumor progression. However, it remains unclear whether CCL15 secreted by tumor cells can also act directly on CCR1 expressed on the same tumor cells to exert tumor-regulatory effects. Here, we discovered that both CCL15 and CCR1 are significantly overexpressed in tumor tissues of patients diagnosed with ESCC. Moreover, baseline expression levels of CCR1 and CCL15 in ESCC cell lines EC109, TE-1, and KYSE150 were markedly higher than those in the normal esophageal epithelial line HET-1A.
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