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.

TRIM22参与肿瘤的发生发展，但其机制尚不清楚。在这项研究中，我们研究了 TRIM22 在胃癌中的表达和生物学作用。我们发现TRIM22 mRNA和蛋白质在胃癌组织和细胞中异常低表达，并与肿瘤大小和浸润深度相关。TRIM22的过表达显着抑制胃癌细胞的增殖、集落形成和迁移，并下调HSPA6的表达。然而，HSPA6-siRNA互补试验表明TRIM22不通过HSPA6调节细胞增殖。此外，TRIM22 的过表达下调了 Smad2 和 Smad3 的磷酸化。此外，TRIM22 直接与 Smad2 结合，Smad2的过表达可以逆转TRIM22对细胞增殖和迁移的抑制作用。在体内，TRIM22 的过表达显着抑制了裸鼠皮下异种移植物的生长。我们的研究表明TRIM22在胃癌的发生发展中具有重要作用，可能通过Smad2抑制胃癌细胞的增殖。