Silencing of SEPT9 inhibits proliferation and migration of endometriotic stromal cells via suppression of the PI3K/AKT signaling pathway.

OBJECTIVE

The aim of this study was to investigate the effects of SEPT9 on proliferation, migration, and apoptosis in endometriotic stromal cells and to explore the underlying mechanisms.

METHODS

Immunohistochemistry and western blotting revealed that SEPT9 expression was significantly elevated in ectopic and eutopic endometrial tissues from patients with endometriosis compared with normal endometrial tissues (p<0.05). Using immortalized human eutopic and ectopic endometrial stromal cells, genetic recombination was applied to overexpress SEPT9 in eutopic cells and knock down SEPT9 in ectopic cells.

RESULTS

Transwell migration, EdU proliferation, and flow cytometry assays showed that SEPT9 overexpression enhanced cell proliferation and migration, whereas SEPT9 silencing reduced these behaviors and increased apoptosis. Pathway analyses identified the PI3K/AKT signaling pathway as a downstream target of SEPT9. Consistently, western blotting and qRT-PCR following SEPT9 knockdown confirmed decreased expression of PI3K/AKT-related proteins and genes.

CONCLUSION

In conclusion, silencing SEPT9 inhibited proliferation and migration and promoted apoptosis in endometriotic stromal cells, potentially through suppression of the PI3K/AKT signaling pathway.