Esm1, also known as endocan, is a secreted protein. It has been implicated in promoting proliferation, angiogenesis, and other oncogenic processes in multiple cancers [1-10]. It is associated with various signaling pathways, such as the Akt pathway, which it activates to drive cancer-related biological functions [1, 4-7].

In ovarian cancer, Esm1 knockdown inhibited cell proliferation, apoptosis escape, the cell cycle, angiogenesis, migration, and invasion. Hypoxia-induced Esm1 upregulation promoted the Warburg effect and vasculogenic mimicry through the PKM2-dependent mechanism [1,2].

In gastric cancer, Esm1 promoted angiogenesis and peritoneal metastasis by binding to c-Met and activating the MAPK/ERK pathway, and also triggered epithelial-to-mesenchymal transition via the EGFR/HER3-Akt/ANGPT2 pathway [3,4].

In colorectal cancer, Esm1 promoted angiogenesis by activating the PI3K/Akt/mTOR pathway [5].

In triple-negative breast cancer, Esm1 promoted cell proliferation through the AKT/NF-κB/Cyclin D1 pathway [6].

In esophageal squamous cell carcinoma, silencing Esm1 suppressed cell proliferation, migration, and invasion [7].

In cervical squamous cell carcinoma, Esm1 overexpression promoted carcinoma angiogenesis and tumor progression through the VEGF/ERK signaling pathway [8].

In conclusion, Esm1 is a crucial factor in promoting cancer-related processes in multiple cancer types, including ovarian, gastric, colorectal, triple-negative breast, esophageal squamous cell, and cervical squamous cell carcinomas. The study of Esm1 using gene knockdown and other functional studies in these cancer models has revealed its significant role in cancer development, progression, and angiogenesis, suggesting it could be a potential therapeutic target and prognostic biomarker for these diseases.