ArticleiScience2025
EPYC promotes laryngeal cancer carcinogenesis and angiogenesis by docking to VEGFR1: A novel therapeutic target.
Article in iScience, 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
EPYC is a member of a small family of leucine-rich repetitive proteoglycans (SLRPs) and contributes to the carcinogenesis of different cancers. However, the role of EPYC in laryngeal cancer (LC) and angiogenesis is still unclear. This study aimed to determine the biological significance of EPYC in laryngeal carcinogenesis and angiogenesis. Here, we found that EPYC was significantly upregulated in LC tissues vs. normal tissues, both in public databases and in in-house LC tissue samples. EPYC knockdown in LC cells attenuated laryngeal carcinogenesis and angiogenesis, while the addition of rhEPYC partially restored tumor growth and neovascularization. Mechanically, EPYC may promote the degradation of VEGFR1 and reduce its ability to act as a decoy of VEGF-A to increase VEGF-A secretion and promote angiogenesis. In conclusion, we showed that EPYC is overexpressed in LC and promotes LC carcinogenesis and angiogenesis by docking to VEGFR1, suggesting EPYC as a novel therapeutic target for LC.
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