Results
| PMID | 25721338 |
| Gene Name | PARK7 |
| Condition | Endometriosis |
| Association |
Associated |
| Population size | 95 |
| Population details | 95 (17 healthy non-menopausal women, 48 patients with ovarian endometriotic cysts, 30 with adenomyosis or normal endometria) |
| Sex | Female |
| Associated genes | DJ-, p-mTOR |
| Other associated phenotypes |
Endometriosis |
|
Gynecol Obstet Invest. 2015;79(3):195-200. doi: 10.1159/000365569. Epub 2015 Feb Guo, Jiubai| Gao, Jumei| Yu, Xiaohong| Luo, Hailian| Xiong, Xiasi| Huang, Ouping Medical Department of Graduate School of Nanchang University, Nanchang, Jiangxi, China. OBJECTIVE: Endometrial cells may aberrantly express molecules involved in invasion and migration, leading to endometriosis. The aim of this study was to investigate the expression of DJ-1 and phosphorylated mammalian target of rapamycin (p-mTOR) in ectopic and eutopic endometria of endometriosis and adenomyosis. METHODS: Endometrial specimens were obtained from healthy non-menopausal women (n = 17) or patients with ovarian endometriotic cysts (n = 48) or adenomyosis (n = 30) during January 2011 to June 2012. The expressions of DJ-1 and p-mTOR were evaluated by immunohistochemistry and western blotting methods. RESULTS: The expressions of DJ-1 and p-mTOR were significantly higher in the ectopic endometria than those in the eutopic endometria of endometriosis and adenomyosis patients or normal endometria (FDR < 0.05). DJ-1 expression was positively correlated with the p-mTOR expression no matter at endometriosis (r = 0.736, FDR < 0.001) or adenomyosis (r = 0.809, FDR < 0.001). CONCLUSION: DJ-1 protein may be involved in endometrial cells proliferation, migration and angiogenesis by modulating the PI3K/Akt/p-mTOR signaling pathway, which provides an underlying theoretical target for endometriosis and adenomyosis. Mesh Terms: Adenomyosis/*metabolism| Adult| Blotting, Western| Endometriosis/*metabolism| Endometrium/*metabolism| Female| Humans| Immunohistochemistry| Intracellular Signaling Peptides and Proteins/*metabolism| Oncogene Proteins/*metabolism| Protein Deglyc |
|