ArticleScientific reports2025
ID1 promotes the progression of esophageal cancer via modulating PTEN/YAP/galectin-3 signaling pathway induced proliferation and immune suppression.
Article in Scientific reports, 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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Abstract
Esophageal cancer (EC) is a highly aggressive malignancy. ID1, a transcription factor overexpressed in multiple cancers, promotes tumor progression, but its molecular mechanisms in EC remain unclear. We hypothesized that ID1 drives EC progression by regulating the PTEN/YAP/Galectin-3 axis to induce proliferation and immune suppression. Bioinformatics analysis was employed to predict and validate the interactions between genes in esophageal cancer; protein expression levels, including ID1 and PTEN, were assessed using western blotting and immunofluorescence; tumor cell proliferation was evaluated with the CCK-8 assay; and macrophage phagocytosis function was tested through engulfment assays. Additionally, the effects of ID1 on esophageal cancer were investigated using subcutaneous tumor transplantation experiments in nude mice and immunohistochemical staining experiments of human cancerous tissues and peritumoral tissues. ID1 was found to inhibit the action of NFIC. When ID1 was overexpressed, there was a decrease in the expression levels of NFIC, PTEN, and p-YAP, and an increase in the levels of Galectin-3, Myc, CD47, and cyclin-A1. Overexpression of ID1 significantly enhanced the proliferation of esophageal cancer cells and improved the phagocytic ability of macrophages, whereas after treatment with PTEN agonists and YAP inhibitors, the proliferation of esophageal cancer cells decreased markedly, and the phagocytic ability of macrophages was reduced. Furthermore, overexpression of ID1 promoted the progression of esophageal cancer, and the expression of ID1 in human cancerous tissues was significantly higher than that in peritumoral tissues. ID1 promotes the progression of esophageal cancer by inducing proliferation and immune suppression through regulation of the PTEN/YAP/Galectin-3 signaling pathway.
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