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Introduction: Gastric cancer (GC) is the sixth most common malignant tumor and the third leading cause of cancer-related death in the world. Studies have shown that TRIM protein can regulate transcription factor activity and is associated with many cancers. However, the role of TRIM11 in gastric cancer remains unclear. Methods: TRIM11 protein levels were examined in 36 cases of GC tissues and 4 gastric cancer cell lines. TRIM11 overexpression and knockdown cells were constructed in MGC-803, HGC-27 and SGC-7901, respectively. The biological roles and mechanisms of TRIM11 were examined using CCK8, colony formation, transwell migration assay, invasion assay, Western blotting, Immunohistochemistry and in vivo nude mice experiments. Results: We found that TRIM11 was upregulated in gastric cancer tissues and gastric cancer cell lines. Functionally, TRIM11 overexpression increased growth rate, colony formation, invasion and migration ability, EMT and β-catenin protein level and its downstream proteins such as CyclinD1 and C-myc, while TRIM11 knockdown shows the opposite effects. Conclusion: In summary, our data show that TRIM11 is overexpressed in GC. TRIM11 promotes proliferation, migration, invasion and EMT of gastric cancer by activating β-catenin signaling. [ABSTRACT FROM AUTHOR]

Gastric cancer (GC) is the sixth most common malignancy and the third leading cause of cancer‐related death worldwide. Emerging evidence suggests that tumour microenvironment cells play a vital role in the development and prognosis of GC. To investigate the possible effect of stromal scores and immune scores on the overall survival (OS) on the GC patients, we divided GC patients into 'high' and 'low' groups based on their stromal and immune scores, and found differentially expressed genes related to prognosis of GC patients. Functional enrichment analysis and GSVA further revealed that focal adhesion and ECM‐receptor interaction are associated with GC patients' survival. Finally, we analysed the effects of genes commonly involved in focal adhesion and ECM‐receptor interaction on GC patients' survival and validated our results in another GC cohort from GEO data sets. In conclusion, we obtained a list of tumour microenvironment‐related genes that predict poor prognosis in GC patients. [ABSTRACT FROM AUTHOR]