Expression and Prognostic Significance of EDIL3 in Gastric Cancer

Abstract Background Epidermal Growth Factor-like repeats and Discoidin I-Like Domains 3 (EDIL3) is a secretory protein that play important roles in embryonic development and various illnesses such as cancer. However, the biological function of EDIL3 in gastric cancer (GC) is still unclear. The objective of this research was to explore the role and potential mechanism of EDIL3 in GC. Methods EDIL3 expression was analyzed using the GEPIA and HPA databases. The prognostic significance of EDIL3 was assessed via the Kaplan–Meier Plotter database. These results were proved by qRT-PCR, Western blot, and Immunohistochemical in our collected GC tissues. To test the function of EDIL3 in GC, shRNA was used to knockdown the EDIL3 expression in two GC lines and several functional experiments were performed. Genetic alterations and DNA methylation were investigated via the cBioPortal, COSMIC, MethSurv, and SMART databases. Upstream regulators of EDIL3 were predicted using RegNetwork. The STRING and GeneMANIA databases were used to analyze the interactive networks for EDIL3. Differential genes correlated with EDIL3 in GC were obtained using LinkedOmics. The relationship between EDIL3 and immune features was analyzed using TIMER, TIMER2.0, and TISIDB databases. The relationship between EDIL3 and drug response was assessed by RNAactDrug database. Results The EDIL3 was highly expressed in GC and associated with adverse clinical features. In vitro assays revealed that EDIL3 promotes the proliferation, migration, and invasion of GC cells. 2.7% of patients harbored EDIL3 mutations and the missense substitution was the most common type. Five CpG sites of EDIL3 were positively related to prognosis in GC. The functions of EDIL3 and co-expression genes were significantly associated with extracellular structure organization and extracellular matrix receptor interaction. EDIL3 expression was positively associated with numerous tumour-infiltrating immune cells and their biomarkers. EDIL3 expression was associated with sensitivity of some GC chemotherapy and targeted drugs. Conclusions This study demonstrated that EDIL3 might function as an oncogene and is associated with immune infiltration in GC. EDIL3 could be used as a potential therapeutic target for GC.