Identification of immune checkpoint inhibitors and biomarkers among STAT family in stomach adenocarcinoma

Background: Gastric cancer is the fifth most prevalent malignancy worldwide, and the third leading cause of cancer-related death. Activating mutations of the JAK/STAT pathway on cellular biological process, inflammation, and immunity of cancer cells have made them promising biomarkers for drug exploitation and malignancy treatment. Specific functions of the STAT family in stomach adenocarcinoma (STAD) have not yet been systematically described. Methods: Bioinformatics web resources, including UALCAN, The Kaplan Meier plotter, and GSCALite, were used to identify immune checkpoint inhibitors and biomarkers among the STAT family in STAD. Results: STAT1, STAT4, STAT5A, and STAT6 were upregulated in STAD at both the mRNA and protein level. STAT1 and STAT5A may act as potential prognostic and prognostic biomarkers in STAD. Among all members of the STAT family, STAT5B (33%), STAT1 (27%), and STAT5A (18%) were the top three frequently mutated genes, and missense mutations were the most common types of genetic alteration. The STAT family has mainly been associated with the activity of several well-known cancer-associated pathways. Low expression of STAT5A and STAT5B were resistant to most of drugs or small molecules in the Genomics of drug Sensitivity in Cancer (GDSC). The functions and pathways of STAT5A in STAD were mainly associated with immune responses, chemokine signaling pathways, and cell adhesion molecules. In addition, we identified several STAT5A associated-targets (transcription factor, kinase, and miRNA targets). Immuno-infiltration analysis suggested a strong association between the STAT5A level, the abundance of immune cells, and the level of immune biomarkers. Conclusions: We identified the immune checkpoint inhibitor and biomarkers among the STAT family in STAD, thereby providing additional information about the significant role of the STAT family in STAD.