TRIM22 inhibits endometrial cancer progression through the NOD2/NF‑κB signaling pathway and confers a favorable prognosis.

Abstract

Endometrial cancer (EnC) is a malignant gynecological tumor commonly observed in developed countries, specifically among post-menopausal women. Although numerous patients with EnC receive promising prognoses, those with advanced or metastatic disease often have a poor prognosis and an impaired quality of life. Tripartite motif-containing 22 (TRIM22) has been confirmed to play many crucial roles in different biological processes, from inflammatory to tumorigenesis. However, the multifaceted roles of TRIM22 in EnC remain uncharacterized. Herein, comparing normal endometrial tissues with tumor tissues obtained from patients, it was concluded that TRIM22 expression was decreased in tumor tissues. However, the overexpression of TRIM22 served to inhibit the migratory, invasive, proliferative and cell cycle activity of EnC cells. Moreover, the knockdown of TRIM22 increased the migratory, invasive, and proliferative activity of the EnC cells. Furthermore, it was found that TRIM22 effectively suppressed EnC progression through the nucleotide binding oligomerization domain containing 2 (NOD2)/nuclear factor (NF)-κB pathway. The data also demonstrated that TRIM22 functions as an inhibitor of EnC tumor xenograft growth in vivo. Overall, the findings of the present study define a novel regulatory role for TRIM22 in EnC progression. Moreover, TRIM22 may serve as an important prognostic predictor for EnC.