TRIM2 directly deubiquitinates and stabilizes Snail1 protein, mediating proliferation and metastasis of lung adenocarcinoma.

Background Lung adenocarcinoma has surpassed lung squamous cell carcinoma as the most common type of non-small cell lung cancer. In this study, we had tested the biological role of TRIM2 in lung adenocarcinoma. Methods TRIM2 abundance in clinical tissues and six cell lines were examined with quantitative real-time PCR test (qRT-PCR) and western blot. TRIM2 overexpression treated H322 cells and TRIM2 knockdown treated A549 cells were used to study cell proliferation, migration, colony formation, invasion, and the expression of epithelial mesenchymal transformation (EMT) biomarkers. Moreover, ubiquitination related Snail1 degradation were studied with qRT-PCR and western blot. The relationships between TRIM2 and Snail1 were investigated with western blot, co-immunoprecipitation, migration, and invasion. Results TRIM2 was highly expressed in lung adenocarcinoma tissues. TRIM2 overexpression and knockdown treatments could affect cell proliferation, colony formation, migration, invasion, and the expression of EMT associated biomarkers. Moreover, TRIM2 can regulate the ubiquitination related Snail1 degradation. In addition, TRIM2 can regulate Snail1 degradation in lung adenocarcinoma via ubiquitination pathway. TRIM2 could promote the proliferation, migration, and invasion of lung adenocarcinoma. Meanwhile, TRIM2 can deubiquitinate and stabilize Snail1 protein, which play important role in the function of lung adenocarcinoma. Conclusion A high TRIM2 expression could be detected in lung adenocarcinoma tissues and cells. TRIM2 could aggravate cell proliferation, invasion, and migration in colorectal cancer by regulating Snail1 ubiquitylation degradation. Our results could provide detailed information for further studies in lung adenocarcinoma.