Depletion of CCL27 inhibits cell proliferation, metastasis and adhesion in ectopic endometrial stromal cells

Endometriosis represents a multifaceted disease with controversial pathogenesis. Effective medical therapy for endometriosis is still urgently needed. In this study, we attempted to reveal the association between CCL27 and endometriosis to investigate new approach in the endometriosis etiology and treatment. We examined the expression of CCL27 in endometriotic tissue and serum samples. Then we analyzed the effects of CCL27 on cell proliferation, migration, invasion, adhesion and signaling pathway in endometrial stromal cells (ESCs) separated from ectopic endometrial tissues after CCL27 knockdown. We found that CCL27 was aberrantly elevated in endometriosis. And the knockdown of CCL27 suppressed endometriosis progression by inhibiting cell growth, metastasis and adhesion in ESCs. And these repressed processes might be mediated by the JAK2/STAT3 pathway inactivated by silencing CCL27 in endometriosis. In conclusion, this study suggests that abnormal expressed CCL27 may function as a stimulative factor in the development of endometriosis.