TRIP 13-dependent pathways promote the development of gastric cancer

TRIP13 is highly expressed in various human tumors and promotes tumorigenesis. We aimed to explore the biological effect of TRIP13 on gastric cancer. The RNA sequence data were retrieved from TCGA to evaluate TRIP13 mRNA expression in gastric cancer. Paired formalin-fixed paraffin-embedded blocks were further analyzed to verify the relationship between TRIP13 expression and carcinogenic status. The functions of TRIP13 on the proliferation of gastric malignancy were investigated by MTT, flow cytometry, colony formation experiment, and nude mouse tumor formation experiment. Finally, microarray analysis of TRIP13-related pathways was performed to identify the potential underlying mechanism of TRIP13 in gastric cancer. TRIP13 was found to have high expression in tumor samples. TRIP13 expression status was significantly subjective to tumor-node-metastasis (TNM) staging and poor survival. The downregulation of TRIP13 promoted apoptosis and inhibited tumor growth. TRIP13-dependent JAK/STAT and NF-κB signaling cascade were found as two key pathways in the carcinogenesis of GC. In conclusion, TRIP13 participates in the carcinogenesis of stomach cancer, and its overexpression in the cancerous tissues dovetail with advanced stage and survival. Moreover, TRIP13 functions as an upstream regulator of the JAK/STAT and p53 signaling pathways, which play critical roles in developing various malignancies. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10142-023-01160-7.