Suppression of PRDX4 inhibits cell proliferation and invasion of ectopic endometrial stromal cells in endometriosis

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Increased PRDX4 expression in ectopic endometria elevates oxidative stress, and its suppression inhibits cell proliferation, invasion, and increases apoptosis in ectopic endometrial stromal cells.

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Abstract

Oxidative stress (OS) has been proposed to play a role in the development of EMs. Peroxiredoxins are a family of antioxidant proteins that exhibit peroxidase activity in a thioredoxin-dependent manner, protecting cells against OS. The Western blotting results showed that the relative expression of PRDX4 was significantly increased in ectopic endometria compared with the normal endometria of EMs-free (p < .05). The H2O2 concentration was also significantly higher in the ectopic endometrium. PRDX4 siRNA was transfected into primary ectopic endometrial stromal cells (EESCs). The viability of the transfected EESCs was measured by CCK-8 assay, and the results showed significantly decreased cell viability. Furthermore, the apoptosis rate and ROS generation in flow cytometry assays were significantly increased after the knockdown of PRDX4 expression (p < .05). Scratch assays and transwell assays revealed that decreased expression of PRDX4 mediated by siRNA inhibited EESC migration and invasion. In conclusion, these findings indicate the potential role of PRDX4 in the development of EMs and PRDX4 as a possible therapeutic target for EMs treatment.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Peroxiredoxins RNA, Small Interfering Case-Control Studies Case-Control Studies Cell Proliferation Cell Proliferation Cell Proliferation Endometriosis Endometriosis Endometriosis Female Female Humans Humans Molecular Targeted Therapy Molecular Targeted Therapy Peroxiredoxins Peroxiredoxins Peroxiredoxins

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References (36)

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