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

Area of Science:

• Oncology
• Molecular Biology
• Biochemistry

Background:

• Gastric cancer (GC) remains a significant global health challenge.
• Understanding the molecular mechanisms driving GC progression is crucial for developing effective therapies.

Purpose of the Study:

• To investigate the role of Tripartite motif-11 (TRIM11) in gastric cancer (GC).
• To explore the association between TRIM11 expression and clinical-pathological features of GC.
• To elucidate the regulatory mechanism of TRIM11 in GC development, focusing on the CPEB3/EGFR axis.

Main Methods:

• Differential expression analysis of TRIM11 in GC tissues versus adjacent normal tissues.
• In vitro assays (CCK-8, colony formation, EdU) to assess cell proliferation after TRIM11 knockdown in GC cell lines (AGS, SGC-7901).
• Western blot analysis and rescue experiments to investigate the involvement of cytoplasmic polyadenylation element-binding protein 3 (CPEB3) and Epidermal Growth Factor Receptor (EGFR) in TRIM11-mediated GC cell proliferation.

Main Results:

• TRIM11 expression was significantly upregulated in GC tissues and correlated with poor prognosis, advanced stage, and larger tumor size.
• Knockdown of TRIM11 suppressed the proliferative potential of GC cells.
• TRIM11 knockdown led to altered protein levels of CPEB3, EGFR, and AKT. Silencing CPEB3 reversed the inhibitory effect of TRIM11 knockdown on GC cell proliferation.

Conclusions:

• TRIM11 is an oncogene in GC, upregulated and associated with adverse clinical outcomes.
• TRIM11 promotes GC cell proliferation by modulating the CPEB3/EGFR signaling pathway.