Is a Potential Prognostic Biomarker in Gastric Cancer and Function as a Tumor Suppressor by Modulating EMT-Related Pathways.

The AT-hook transcription factor, AKNA, is a nuclear protein that affects a few physiological and pathological processes including cancer. Here, we investigated the role of in gastric cancer (GC). By using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assays, was found deregulated in both GC cell lines and 32 paired GC tissues. Subsequently, Kaplan-Meier analysis and clinicopathological analysis were conducted using both 32 GC cases' data above and RNA-Seq data of in 354 GC patients and the corresponding clinical-pathological data obtained from The Cancer Genome Atlas (TCGA), and expression was found closely related to location, metastasis, and TNM staging of GC. Then, the potential molecular mechanisms of in GC were explored by gene set enrichment analysis (GSEA), qRT-PCR, and Western blot assays. was found to be a hub gene related to homotypic cell to cell adhesion, regulation of cell to cell adhesion, leukocyte cell to cell adhesion, and regulation of T cell proliferation in GC. GO analysis revealed that involved in the regulation of epithelial-mesenchymal transition (EMT)-related pathways including chemokine signaling pathway, cytokine to cytokine receptor interaction, cell adhesion molecules, and jak-stat signaling pathway in GC. To explore the regulation of expression, and were used to predict the possible miRNA which targeted and found the expression of was negatively correlated to miR-762 which could be sponged by circTRNC18. In conclusion, could function as a tumor suppressor by modulating EMT-related pathways in GC. The expression of might be regulated by circTRNC18/miR-762 axis. could serve as a potential biomarker and an effective target for GC diagnosis and therapy.