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Background Filaggrin (FLG) plays an important role in the progression of malignant tumors; however, its expression characteristics and biological functions in gastric cancer (GC) remain unclear. Methods Cancer-related datasets were retrieved from public repositories, including the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA). A competing endogenous RNA (ceRNA) network was constructed to explore potential regulatory networks involving FLG. Differential expression analysis, genetic alteration analysis, and clinicopathological and survival analyses were performed to evaluate the role of FLG in GC. In addition, Gene Set Enrichment Analysis (GSEA), immune infiltration analysis, and in vitro functional experiments were conducted to investigate the biological effects and potential mechanisms of FLG in GC. Results FLG was aberrantly expressed across multiple cancer types and was significantly associated with clinical characteristics and prognosis in GC. Further analyses showed that FLG was involved in genetic alterations and was closely associated with the immune microenvironment in GC. Functional experiments demonstrated that FLG promoted the invasion and metastasis of GC cells. Mechanistically, GSEA and experimental validation indicated that FLG exerted its tumor-promoting effects, at least in part, through activation of the epithelial-mesenchymal transition (EMT) signaling pathway. Conclusion This study clarifies the biological role of FLG in GC and highlights its potential as a novel prognostic biomarker and therapeutic target. These findings provide new insights into the molecular mechanisms underlying GC progression and may contribute to the development of more effective diagnostic and therapeutic strategies.
Xia et al. (Fri,) studied this question.