CEACAM7 Promotes Tumor Progression by Regulating GCNT3 Expression in Lung Adenocarcinoma

Background: Lung adenocarcinoma (LUAD) is a global epidemic with extremely high lethality, yet its exact molecular mechanisms remain under-explored. Therefore, the study of molecular regulators of the developmental process of LUAD is of crucial importance for developing innovative therapeutic approaches to enhance the survival rate of individuals with LUAD. Methods: Through bioinformatics analyses of several public gene databases, we thoroughly examined the expression, clinical significance, co-expressed genes, and signal transduction pathways of CEACAM7 in LUAD. Reverse transcription quantitative PCR (RT-qPCR) and Western blotting (WB) were utilized to detect the CEACAM7 expression in clinical LUAD tissues. The CCK-8 method, WB, colony formation, Transwell, wound healing, and immunoprecipitation assays were utilized to explore the molecular mechanism of CEACAM7′s role in LUAD. The tumorigenic role of CEACAM7 was further validated in vivo in a subcutaneous xenograft model established in female BALB/c nude mice (n = 5 per group). Results: CEACAM7 is significantly overexpressed in LUAD, and its upregulation is linked to tumor aggressiveness and poor prognosis. Our experimental results suggest that regulation of CEACAM7 expression, either through up- or down-regulation, results in enhancement or suppression of growth and invasion of H1650 cells, respectively. In H1650 cells, CEACAM7 was shown to directly interact with GCNT3 and trigger growth and invasion of H1650 cells and epithelial–mesenchymal transition (EMT). In vivo, knockdown of CEACAM7 significantly suppressed xenograft tumor growth in nude mice. Conclusions: Our findings demonstrating the biological function of CEACAM7 in LUAD both in vitro and in vivo provide new insights and underline its capability as a predictive biomarker and therapeutic target.