TREM1 PROMOTES GASTRIC CANCER METASTASIS AND LEADS TO POOR PROGNOSIS IN PATIENTS THROUGH THE ERK/IL-6 SIGNALING PATHWAY

Objective: To analyze the expression of TREM1 in gastric cancer tissues and serum of gastric cancer patients, and to explore the link between TREM1 expression levels and the clinical features of patients. Furthermore, to explore the specific mechanism by which TREM1 promotes the metastatic ability of MKN45 cells. Method: Gene expression analysis, differential genes, KEGG enrichment analysis, and immune correlation analysis were performed using TCGA and GEO databases; Compare the concentration of TREM1 in the serum of gastric cancer patients using clinical serum sample standards and group them to analyze the relationship between TREM1 and clinical characteristics and prognosis of patients; Select MKN45 cells, silence the expression of TREM1 and IL-6 using small interfering RNA, overexpress TREM1 using plasmid, and perform corresponding treatments. Compare the changes in cell proliferation and migration ability in different groups using scratch assay and transwell assay; Western blotting was used to detect changes in the ERK signaling pathway, IL-6 expression, and EMT related proteins among different groups; Real time fluorescence quantitative PCR comparison of changes in downstream immune factors of TREM1. Result: TREM1 concentration increased in the serum of gastric cancer patients and was associated with their recurrence, metastasis, and overall survival time; TREM1 promotes invasion and metastasis of MKN45 cells; TREM1 upregulates IL-6 by activating the ERK signaling pathway; TREM1 promotes gastric cancer EMT by upregulating IL-6, leading to enhanced metastatic ability of gastric cancer cells. Conclusion: TREM1 is highly expressed in the serum of gastric cancer patients and upregulates IL-6 by activating the ERK signaling pathway, thereby promoting EMT and invasion and metastasis of gastric cancer, leading to poor prognosis for patients.