| Popis: |
Background: Although SNORD3A has been implicated in cancer progression, its specific roles and underlying mechanisms in gastric cancer (GC) remain poorly understood. We analysed SNORD3A expression using TCGA data and evaluated patient survival via Kaplan‒Meier curves. Additionally, we conducted GO-KEGG enrichment analysis to identify relevant biological processes and signaling pathways, while ssGSEA was used to assess the correlation between SNORD3A and cancer immune infiltrates. Furthermore, we explored the relationship between SNORD3A and immunotherapy response through TIDE. We verified SNORD3A expression using real-time qPCR and assessed cell proliferation, migration, and invasion via CCK8 and Transwell migration and invasion assays. Results: Our results revealed that SNORD3A was significantly upregulated in GC, with high expression correlating with poor survival. SNORD3A and related genes were primarily enriched in the insulin/insulin-related growth factor signaling pathway. We also observed negative associations between SNORD3A expression and several immune cells, including activated dendritic cells, CD56bright natural killer cells, central memory CD8 T cells, effector memory CD8 T cells, effector memory CD4 T cells, eosinophils, immature dendritic cells, macrophages, mast cells, MDSCs, memory B cells, monocytes, neutrophil cells, plasmacytoid dendritic cells, regulatory T cells, and T follicular helper cells. High SNORD3A expression also correlated with a poorer response to immunotherapy. Finally, inhibition of SNORD3A suppressed cell proliferation, migration, and invasion. Conclusions: Our findings suggest that SNORD3A plays a catalytic role in the proliferation, migration and invasiveness of GC and may have potential as a diagnostic biomarker and therapeutic target for GC.How to cite: Wang Q, Li Y, Niu X, et al. SNORD3A acts as a potential prognostic and therapeutic biomarker in gastric cancer. Electron J Biotechnol 2023; 67. https://doi.org/10.1016/j.ejbt.2023.08.004. |
