TRIM11 stimulates the proliferation of gastric cancer through targeting CPEB3/EGFR axis.

Purpose: To explore the relationship between TRIM11 (Tripartite motif-11) level and clinical pathology of gastric cancer (GC), as well as its regulatory role in the development of GC. Methods: Differential expression of TRIM11 in GC and pa- racancer tissues was determined. The relationship between TRIM11 level and clinical pathology of GC patients was assessed. After knockdown of TRIM11, changes in the pro- liferative potentials of AGS and SGC-7901 cells were exam-ined by cell counting kit-8 (CCK-8), colony formation and 5-Ethynyl-2'-deoxyuridine (EdU) assay. The cytoplasmic polyadenylation element-binding protein 3 (CPEB3) level in GC species was tested and its regulatory role in viability of GC cells was explored as well. The involvement of CPEB3/ EGFR axis in TRIM11-regulated proliferative ability of GC was detected by Western blot and rescue experiments. Results: TRIM11 was upregulated in GC species and its high level was related to poor prognosis, advanced pathologi-cal stage and large GC tumor size. Knockdown of TRIM11 attenuated the proliferative potential of GC cells. Protein level of CPEB3 was upregulated, while EGFR and AKT were downregulated in GC cells with TRIM11 knockdown. Moreo- ver, CPEB3 was lowly expressed in GC samples and notably, knockdown of CPEB3 abolished the inhibitory effect of si- lenced TRIM11 on the proliferative potential of GC. Conclusions: TRIM11 is upregulated in GC and correlated to prognosis, pathological stage and GC tumor size. TRIM11 triggers the proliferative potential of GC through regulating CPEB3/EGFR axis.