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Endothelial cell-specific molecule 1 (ESM1), also known as endocan, is a secreted, cysteine-rich dermatan sulfate proteoglycan highly expressed by endothelial cells, especially in the lung and kidney[4]. ESM1 is encoded by the *ESM1* gene on chromosome 5q11.2 and is regulated by cytokines and growth factors. It consists of a 20 kDa protein core (mature: 165 amino acids) and a dermatan sulfate glycosaminoglycan chain[1][2]. ESM1 plays a key role in the regulation of cell adhesion, migration, promoting angiogenesis, modulating inflammation, and influencing neutrophil and leukocyte trafficking via interaction with integrins and VE-cadherin. Overexpression and secretion of ESM1 are frequently observed in a variety of cancers, where it contributes to tumor growth, angiogenesis, enhanced metastasis, and therapy resistance by activating several signaling pathways (notably PI3K-Akt, NF-κB, VEGF-A/VEGFR-2, Wnt/β-catenin, and EMT). ESM1 is being studied as both a prognostic biomarker and a potential therapeutic target in oncology, inflammation, cardiovascular, and renal diseases[2][3][4][1].
Anti-ESM1 antibodies may inhibit cancer cell proliferation, migration, angiogenesis, and metastasis via blocking PI3K/Akt, NF-κB, EMT, and VEGF/VEGFR-2 pathways[2][3]. Antisense oligonucleotides or other knockdown strategies reduce ESM1 expression, leading to inhibition of tumor progression and improved apoptosis[3].
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