<p>Quercetin Inhibits Adenomyosis by Attenuating Cell Proliferation, Migration and Invasion of Ectopic Endometrial Stromal Cells</p>

Abstract

To evaluate the effects of quercetin on proliferation, invasion and migration of endometrial stromal cells (ESCs) from adenomyosis patients. Methods: Primary ectopic ESCs (EESCs) and eutopic ESCs (EuESCs) were obtained and purified from patients undergoing total hysterectomy for adenomyosis and identified by immunocytochemistry staining. The cytotoxicity and inhibition rate were determined by CCK-8 assay to obtain the IC 50 value. Cell proliferative, migratory, and invasive abilities were detected by BrdU, wound scratch, transwell assays, respectively. Western blot analysis was employed to explore the effects of quercetin on the expression of MMP-2, MMP-9, Ezrin and Fascin proteins in cells. Results: Both EESCs and EuESCs were characterized with strongly positive staining for vimentin and almost negative for cytokeratin. Quercetin inhibited the viability of EESCs and EuESCs in a dose-and time-dependent manner, with an IC 50 = 33.00 μM for EuESCs and IC 50 = 74.88 μM for EESCs at 72 h. Thus, the final concentrations and action time of quercetin in EuESCs (0, 20, 40, and 80 μM for 72 h) and EESCs (0, 40, 80, and 160 μM for 72 h) were selected. BrdU assay showed that quercetin dose-dependently suppressed the proliferation of EESCs and EuESCs, while the inhibition rate in EESCs was higher. Similarly, administration of quercetin in EESCs and EuESCs significantly decreased the motility and invasiveness in a dose-dependent fashion, with stronger inhibitory effects on EESCs. Finally, Western blot analysis demonstrated that invasion-and migration-related proteins (MMP-2, MMP-9, Erzin, and Fascin) were significantly downregulated with the quercetin concentration increasing. Moreover, the decreased level of these proteins in EESCs under quercetin exposure was greater than that in EuESCs. Conclusion: Quercetin can inhibit the proliferation of EESCs in adenomyosis and reduce their mobility and invasiveness. These inhibitory effects may be related to the downregulation of MMP-2, MMP-9, Fascin, and Erzin proteins.

Follistatin is a crucial chemoattractant for mouse decidualized endometrial stromal cell migration by JNK signalling

“…MMP2, MMP9 and ezrin are known to be involved in cell migration, and vimentin is an important marker for mesenchymal/motile phenotype 30,31 . Therefore, to determine the mechanism of action of activin A and FST on d‐MESCs migration, MMP2, MMP9, Vimentin and Ezrin expressions were analysed by Western blotting.…”

“…MMP2, MMP9 and ezrin are known to be involved in cell migration, and vimentin is an important marker for mesenchymal/motile phenotype. 30 , 31 Therefore, to determine the mechanism of action of activin A and FST on d‐MESCs migration, MMP2, MMP9, Vimentin and Ezrin expressions were analysed by Western blotting. The results showed that the expressions of MMP9 and Ezrin were upregulated significantly after FST stimulation, and only slightly increased after activin A treatment (Figure 4A ).…”

Polypeptide induced perylene probe excimer formation and its application in the noncovalent ratiometric detection of matrix metalloproteinase activity

“…The above screening results are consistent with the literature. 46–49 These inhibitors have been demonstrated in diseases related to matrix metalloproteinases, indicating that the method can be applied to the screening of MMP inhibitors.…”

Circ_0061140 Facilitates Adenomyosis Progression by Upregulating LIN28B in vitro

“…As a result, miR-141-3p was confirmed as a downstream molecule of circ_0061140. Increasing studies showed that cell migration and invasion played important roles in the pathogenesis of adenomyosis [38-40]. Accumulating evidence has revealed that miR-141-3p suppressed cell motility of tumor cells in multiple malignancies [41-43].…”