Association of matrix metalloproteinase-3 with transforming growth factor-β1 mediated increased cellular invasion in ovarian endometriosis
OA: closed
CC0
Abstract
Endometriosis is an estrogen-dependent gynecological disease, where ectopic growth of endometrial tissues causes severe pain and infertility. The pathophysiology of endometriosis involves cellular invasion and transitions such as epithelial-mesenchymal transition (EMT). Matrix metalloproteinase (MMP)-3 and transforming growth factor (TGF)-β pathway are two important regulators of the process. In this report, we studied 12 control women without endometriosis and 24 women with ovarian endometriosis (12 early and 12 late stages) for evaluation of serum and tissue levels of MMP3 and TGFβ1. Serum levels of MMP3 and TGFβ1 were significantly elevated in patients with endometriosis compared to control women. Late stage (III and IV) endometriosis patients displayed significantly higher levels of serum MMP3 and TGFβ1 than early stage (I and II) patients. We found a positive correlation between serum MMP3 and TGFβ1 levels. Ectopic endometriotic tissues exhibited higher MMP3 expressions as compared to eutopic endometrium and were increasingly expressed with severity of the disease. In vitro studies using Chinese hamster ovarian epithelial (CHO) cells found TGFβ1 treatment upregulated MMP3 levels. TGFβ1 treatment promoted cellular invasion of CHO cells in a MMP dependent manner. Present study highlights an association of MMP3 in TGFβ1-mediated promotion of cellular invasion in endometriosis.
My notes (saved in your browser only)
Citation neighborhood (2-hop)
Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]
References (29)
- Association of <i>MMP7</i> (−181A > G) promoter polymorphism with endometriosis in Eastern Indian women via openalex
- Effects of matrix stiffness on epithelial to mesenchymal transition-like processes of endometrial epithelial cells: Implications for the pathogenesis of endometriosis via openalex
- EGFR-mediated matrix metalloproteinase-7 up-regulation promotes epithelial-mesenchymal transition via ERK1-AP1 axis during ovarian endometriosis progression via openalex
- Endometriosis and the neoplastic process via openalex
- Endometriosis: pathogenesis and treatment via openalex
- Endometriosis Typology and Ovarian Cancer Risk via openalex
- Epithelial-Mesenchymal Transition in Endometriosis-When Does It Happen? via openalex
- Epithelial-to-mesenchymal transition contributes to the downregulation of progesterone receptor expression in endometriosis lesions via openalex
- Epithelial-to-mesenchymal transition in the development of endometriosis via openalex
- Micrometastasis of endometriosis to distant organs in a murine model via openalex
- New Evidence About Malignant Transformation of Endometriosis-A Systematic Review via openalex
- Regulation of Matrix Metalloproteinase-2 Activity by COX-2-PGE2-pAKT Axis Promotes Angiogenesis in Endometriosis via openalex
- Role of melatonin in regulating matrix metalloproteinase-9 via tissue inhibitors of metalloproteinase-1 during protection against endometriosis via openalex
- The involvement of multifunctional TGF-β and related cytokines in pathogenesis of endometriosis via openalex
- The role of fibrosis in endometriosis: a systematic review via openalex
- The Role of Matrix Metalloproteinases in Endometriosis: A Potential Target via openalex
- The role of TGF-β in the pathophysiology of peritoneal endometriosis via openalex
- W3019034047 via openalex
- W1760215417 via openalex
- W2171875732 via openalex
- W2125681453 via openalex
- W4225698268 via openalex
- W4394747404 via openalex
- W2072503088 via openalex
- W2071359561 via openalex
- W1977000581 via openalex
- W4409973304 via openalex
- W4412990463 via openalex
- W1968044382 via openalex
Source provenance
- openalex
- last seen: 2026-10-30T06:01:36.263981+00:00
- unpaywall
- last seen: 2026-10-30T06:30:42.975179+00:00
License: CC0
· commercial use OK