Tumor‐derived endomucin promotes colorectal cancer proliferation and metastasis

Abstract Background Endomucin (EMCN) is a type I transmembrane glycoprotein and a mucin‐like component of the endothelial cell glycocalyx. The mechanism of EMCN action in colorectal cancer (CRC) remains unclear. Aims Our aim was to explore the role of EMCN in the progression of CRC. Materials & Methods We examined EMCN expression in CRC tissues and normal para‐carcinoma tissues. The function and mechanisms of EMCN were checked in CRC cell lines and in mouse xenograft. Additionally, we used co‐immunoprecipitation and mass spectrometry to identify the potential EMCN‐binding proteins. Functional annotation analysis showed where these genes were enriched. Results We found that EMCN was overexpressed in tumor tissues compared with that in normal para‐carcinoma tissues. We also found that overexpression of EMCN induced CRC proliferation and metastasis both in vitro and in vivo. EMCN knockdown prevents epithelial‐mesenchymal transition in vitro. We identified 178 potential EMCN‐binding partners. Furthermore, functional annotation analysis indicated that these genes were considerably enriched in carcinogenic‐related functions and pathways. Collectively, the identification of EMCN‐binding partners enhanced our understanding of the mechanism of EMCN‐mediated malignant phenotypes, and this research may provide valuable insights into the molecular mechanisms underlying CRC. Conclusion Tumor‐derived endomucin promotes colorectal cancer proliferation and metastasis. We identified 178 EMCN‐binding proteins and initially screened three potential EMCN‐interacting proteins: NALCN, and TPM2, ANKK1. Our study provides valuable insights into the molecular mechanisms underlying CRC development.