Estrogen-increased SGK1 Promotes Endometrial Stromal Cell Invasion in Adenomyosis by Regulating with LPAR2

Adenomyosis is an estrogen-dependent gynecological disorder. The abnormal migration and invasion of the eutopic endometrium is thought to be the primary role in the pathogenesis of adenomyosis. However, the exact underlying mechanism remains unclear. This study investigated involvement of serum and glucocorticoid-regulated kinase 1 (SGK1) in the pathogenesis of adenomyosis. The SGK1 expression level was higher in the eutopic endometrium of adenomyosis. Upregulation of SGK1 can promote the migration, invasion of human stromal endometrial cells (HESC). Through RNA sequencing and other technical methods, we found that SGK1 regulates the expression of the important downstream molecule Lysophosphatidic acid receptor 2 (LPAR2), and ultimately regulates the expression level of functional proteins such as matrix metalloproteinase 2 and matrix metalloproteinase 9, which are related to migration and invasion. Then, we found that 17 beta-estradiol (E-2) upregulated the expression of SGK1 in endometrial cells in a dose-dependent manner. Furthermore, SGK1 shRNA significantly suppressed the migration and invasion induced by E-2 in endometrial cells, as well as the related factors. Our study revealed the possible role of SGK1 in the migration and invasion in the development of adenomyosis.

Automated summary

The study revealed higher expression of serum and glucocorticoid-regulated kinase 1 (SGK1) in adenomyosis, which promotes cell migration and invasion by regulating downstream molecules and proteins.