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Cite this article
Effect of Wnt/β-catenin signal pathway on of matrix metalloproteinase-7 and vascular endothelial growth factor gene expressions in endometriosis
1 Department of Obstetrics and Gynecology, Zhengzhou People’s Hospital, Zhengzhou City
2 Department of Obstetrics and Gynecology, Women & Infants Hospital of Zhengzhou, Zhengzhou City
3 Department of Equipment, Zhengzhou People’s Hospital, Zhengzhou City
4 Department of Obstetrics and Gynecology, University Hospital of Hubei University For Nationalities, Enshi City
5 Department of Gynecology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou City (China)
Clin. Exp. Obstet. Gynecol. 2016, 43(4), 573–577; https://doi.org/10.12891/ceog3053.2016
Published: 10 August 2016
Purpose: To explore the function of Wnt/β-catenin signal pathway on promoting the adhesion, invasion, and metastasis of endometriosis tissues by analyzing its effects on the expressions of matrix metalloproteinase-7 (MMP-7) and vascular endothelial growth factor in endometriosis. Materials and Methods: Endometriosis nude mice models were included. Small RNA interference technology was used to block Wnt/β-catenin signal pathway. HE staining technique was adopted to observe the difference of pathological morphology among groups. The immunohistochemistry and real-time quantitative PCR were performed to analyze the expressions of β-catenin, MMP-7 and VEGF from protein and mRNA levels. Results: Whether the Wnt/β-catenin signal pathway was blocked or not had little effect on the pathological morphology of lesions. The expressions of β-catenin, MMP-7 and VEGF in siRNA group were much lower than those in negative control group and control group (p < 0.05), while there was no statistical significance in the difference of expressions between negative control group and control group (p > 0.05). Conclusion: Blocking of Wnt/β-catenin signal pathway caused the decrease of MMP-7 and VEGF expressions, indicating that Wnt/β-catenin signal pathway plays an important role in the adhesion, invasion, and metastasis of endometriosis tissues.