The cGAS-STING pathway promotes endometriosis by up-regulating autophagy

To investigate the roles of the cGAS-STING signal pathway and autophagy in the disease progression of endometriosis and to explore the regulatory mechanism of the cGAS-STING signal pathway on autophagy.

A case-control experimental study, in vitro primary cell culture study, and in vivo animal research.

Immunohistochemistry, RT-PCR and Western Blot were used to detect cGAS-STING signal pathway and autophagy expression differences in human and rat models. The lentivirus was used to overexpress STING in cells. The expression level of autophagy in human endometrial stromal cells (HESCs) transfected with lv-STING was detected by Western Blot, RT-PCR, and immunofluorescence. Transwell migration and invasion assays were conducted to assess cellular motility. The STING antagonist was applicated in vivo to investigate the therapeutic effects.

The expression levels of the cGAS-STING signal pathway and autophagy in Human and Rat ectopic endometrium were increased. STING overexpression promotes the expression of autophagy in human endometrial stromal cells (HESCs). STING overexpression enhances the migration and invasion of the human endometrial stromal cells (HESCs), but the addition of autophagy antagonists could significantly reverse this. STING antagonists inhibited the expression of autophagy in vivo and reduced the volume of ectopic lesions.

The expression levels of the cGAS-STING signal pathway and autophagy were increased in endometriosis. cGAS-STING signal pathway promotes the development of endometriosis by upregulating autophagy.