Abstract
Objective
Endometriosis is an estrogen-dependent disease, a steroid receptor-binding protein
bearing the regulator of the G-protein signaling domain (SRB-RGS) can suppress the
estrogen receptors-mediated transcriptional activities. We sought to determine whether
overexpression of SRB-RGS suppresses the migration and invasion ability of endometrial
stromal cells stimulated by 17β-estradiol (E2).
Study Design
Endometrial stromal cells were obtained from endometriosis patients. SRB-RGS was overexpressed
in the cells stimulated by E2. The migration and invasion ability of the cells were
measured by migration assay and invasion assay, respectively. Western blot analysis
was done to test the expression of matrix metalloproteinase-9 (MMP-9), tissue inhibitors
of metalloproteinase-1 (TIMP-1) and vascular endothelial growth factor (VEGF).
Results
Overexpression of SRB-RGS suppressed the migration and invasion ability of the stromal
cells stimulated by E2; it also suppressed the expression of MMP-9 and VEGF, while
the expression of TIMP-1 was increased.
Conclusions
Overexpression of SRB-RGS suppresses the migration and invasion ability of the E2-stimulated
endometrial stromal cells. The molecular mechanism is the reduced expression of MMP-9
and VEGF, and the increased expression of TIMP-1. These findings suggest that the
coding gene of SRB-RGS is a promising target gene for endometriosis gene therapy.
Keywords
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Article info
Publication history
Published online: November 24, 2015
Accepted:
November 18,
2015
Received in revised form:
November 13,
2015
Received:
May 27,
2015
Identification
Copyright
© 2015 Elsevier Ireland Ltd. Published by Elsevier Inc. All rights reserved.
