Inhibiting CSNK2A Suppresses the Viability, Autophagy, Growth and Motility of Ectopic Endometrial Stromal Cells

Endometriosis is an estrogen-dependent disorder characterized by ectopic growth of endometrial tissue. There is a lack of effective biomarkers for early detection and revealing mechanisms of endometriosis. CSNK2A1 is a compositionally active serine/threonine protein kinase that exerts its role by phosphorylating a variety of substrates, however, the role and mechanism of CSNK2A1 in endometriosis progression is still unclear. The aim of this study was to uncover the role of CSNK2A1 in endometriosis and elucidate the relevant mechanisms. Herein, we found CSNK2A1 is highly expressed in endometriosis. Its depletion inhibited the activity of ectopic endometrial stromal (ESC) cells. Further, knocking down of CSNK2A1 restrained the motility of ESC cells, and its ablation contributed to the autophagy of ESC cells. Mechanically, the depletion of CSNK2A1 blocked the PI3K/Akt/mTOR pathway in ESC cells. In summary, CSNK2A ablation inhibited the viability, autophagy, proliferation and invasion of ectopic endometrial stromal cells via targeting PI3K/Akt/mTOR pathway.