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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  AKNA  in gastric cancer (GC). By using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assays,  AKNA  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  AKNA  in 354 GC patients and the corresponding clinical-pathological data obtained from The Cancer Genome Atlas (TCGA), and  AKNA  expression was found closely related to location, metastasis, and TNM staging of GC. Then, the potential molecular mechanisms of  AKNA  in GC were explored by gene set enrichment analysis (GSEA), qRT-PCR, and Western blot assays.  AKNA  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  AKNA  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  AKNA  expression,  Targetscan  and  TargetMiner  were used to predict the possible miRNA which targeted  AKNA  and found the expression of  AKNA  was negatively correlated to miR-762 which could be sponged by circTRNC18. In conclusion,  AKNA  could function as a tumor suppressor by modulating EMT-related pathways in GC. The expression of  AKNA  might be regulated by circTRNC18/miR-762 axis.  AKNA  could serve as a potential biomarker and an effective target for GC diagnosis and therapy.

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