Tanshinone IIA inhibits the proliferation, migration and invasion of ectopic endometrial stromal cells of adenomyosis via 14-3-3ζ downregulation.

BACKGROUND

Adenomyosis is a specific subtype of endometriosis and recent evidences have indicated that Tanshinone IIA (TSIIA) might be a potential therapeutic option for endometriosis. Meanwhile, endometrial stromal cells (ESCs) of adenomyosis might play crucial roles in the progression of this disease, emphasizing the importance of targeting ESCs in the treatment of adenomyosis. Furthermore, previous evidences also implicated that deregulated 14-3-3ζ expression might be associated with therapeutic effects of certain drugs.

AIM OF THE STUDY

The aim of this study is to evaluate the potential involvement of 14-3-3ζ in the process of TSIIA-treated adenomyosis.

MATERIALS AND METHODS

Ectopic endometrial stromal cells (EESCs) were isolated from a total of 3 patients with adenomyosis. Cells were treated with TSIIA and infected with 14-3-3ζ-overexpressing adenovirus, the expression level of 14-3-3ζ was determined by western blotting (WB), cell viability was detected by Cell Counting Kit-8 (CCK8), cell invasion and migration was evaluated by transwell assay, and cell apoptosis was detected by flow cytometry.

RESULTS

TSIIA could decrease cell viability, induce cell apoptosis, and inhibit cell migration and invasion in EESCs. Mechanistically, TSIIA markedly reduced the expression of 14-3-3ζ in EESCs, and overexpression of 14-3-3ζ could restore the ability of cell viability, migration and invasion, but has no effect on cell apoptosis.

CONCLUSIONS

TSIIA could be a promising novel therapeutic agent for adenomyosis, via inducing cell apoptosis, inhibiting cell viability, migration and invasion in EESCs. Furthermore, the effects of cell viability, migration and invasion were mediated in 14-3-3ζ-dependent manner while that of cell apoptosis was mediated in 14-3-3ζ-independent manner.