Abstract
TRIM22 is involved in tumorigenesis and development, but its mechanism is not clear. In this study, we investigated the expression and biological role of TRIM22 in gastric cancer. We found that TRIM22 mRNA and protein expression was abnormally low in gastric cancer tissues and cells and correlated with tumor size and depth of invasion. Overexpression of TRIM22 significantly inhibited the proliferation, colony formation, and migration of gastric cancer cells and downregulated the expression of HSPA6. However, the HSPA6-siRNA complementation test showed that TRIM22 did not regulate cell proliferation through HSPA6. Furthermore, overexpression of TRIM22 downregulated the phosphorylation of Smad2 and Smad3. In addition, TRIM22 directly binds to Smad2, and overexpression of Smad2 can reverse the inhibition of cell proliferation and migration induced by TRIM22. In vivo, overexpression of TRIM22 significantly inhibited the growth of subcutaneous xenografts in nude mice. Our study indicates that TRIM22 has an important role in the development of gastric cancer and may inhibit the proliferation of gastric cancer cells through Smad2.
Highlights
Gastric cancer is one of the most common malignant tumors worldwide and has a poor prognosis
We found that the expression of Tripartite motif-containing 22 (TRIM22) protein and mRNA decreased in gastric cancer cell lines compared with that in the immortalized normal gastric epithelial cell line GES-1 (P < 0.01, Fig. 1C)
Recent studies have reported that TRIM22 plays a role in lung cancer and leukemia, which indicates that TRIM22 may be involved in the regulation of malignant tumors
Summary
Gastric cancer is one of the most common malignant tumors worldwide and has a poor prognosis. Recent studies have shown that TRIM22 is involved in cell differentiation and proliferation and might play a role in the development of some tumors. TRIM22 expression was upregulated in non-small-cell lung cancer and promoted the proliferation, colony formation, and invasion of A549 cells while inducing epithelial–mesenchymal transition (EMT) via the Akt/GSK-3β/β-catenin signaling pathway [13]. Knockdown of TRIM22 expression inhibited proliferation and invasion and significantly induced cell cycle arrest by regulating CDK4, cyclin D1, P70S6K, and p53 expression in chronic myelogenous leukemia cells [14]. These results suggest that TRIM22 may have a role in tumorigenesis and development. The role of TRIM22 in gastric cancer remains unclear
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
