Abstract
Although the medical science has been developed for decades, the molecular mechanism of endometrial cancer (EC) is not yet completely clear. Previous studies have shown that the tripartite motif containing 28 (TRIM28) plays a crucial role in tumor development. However, TRIM28 is rarely studied in EC, and its role and mechanism need to be further determined. This study was aimed to delve into the related molecular mechanism underling the role of TRIM28 in EC cell growth and migration. qPCR assays and Western blot assays revealed that the expression level of TRIM28 was higher in EC tissues or cell lines (HEC1B, AN3CA, and Ishikawa) than normal tissue or human endometrial epithelial cells (hEEC), respectively. Then, CCK-8 cell viability assay and clone formation assay were performed in HEC1B and AN3CA cell lines after overexpression or knockdown of TRIM28. The results verified that suppression of TRIM28 expression inhibited the proliferation of EC cells. The wound scratch healing assay and transwell assay were performed in HEC1B and AN3CA cell lines after overexpression or knockdown of TRIM28. The results showed that suppression of TRIM28 expression inhibited the invasion and migration of EC cells. Finally, the Western blot assays hinted that overexpression or knockdown of TRIM28 in HEC1B and AN3CA cell lines would promote or inhibit the phosphorylation of AKT and mTOR protein. These findings indicated that TRIM28 promoted the growth and migration of EC cells via regulating the AKT/mTOR pathway.