Cancer-associated fibroblasts promote esophageal carcinogenesis and lung metastasis by CDH11
Calreticulin CDH11 is exclusively expressed in these CAFs and upregulated in conjunction with lung metastasis of ESCC. CDH11 modulates the AKT-related signaling pathway through its interaction with FGFR1, influencing CAF-mediated extracellular matrix remodeling, thereby facilitating metastatic progression. Application of the CDH11 inhibitor, celecoxib, presents a promising new strategy for targeting lung metastasis in ESCC. The molecular mechanisms underlying the lung metastatic microenvironment of ESCC, which are expected to improve the molecular typing accuracy of ESCC lung metastasis to the single-cell level contribute to the development of a precision therapeutic system based on the modulation of the stromal microenvironment, with significant clinical translational potential.