Does T-cadherin have a role in endometriosis?Feb 4, 2020
A novel research on with potential theraupetic implications: T-cadherin in endometriosis
- There is currently no valid biomarker for endometriosis.
- A molecule named "T-cadherin" controlling migration and invasion in different cancers, has not been explored in endometriosis yet.
- Downregulation of T-cadherin, a molecule from the cadherin family, is related to the invasion and metastasis of malignant tumors.
- Data in this research provide new insights into the pathogenesis of endometriosis, and most importantly T-cadherin may be a new potential therapeutic target in endometriosis.
What's done here:
- The expression of T-cadherin(n=40) with and without endometriosis (n= 24) was investigated.
- Invasion, migration and signaling pathway regulation of T-cadherin overexpression were also studied on isolated endometrial stromal cells.
- No difference was found in the expression of T-cadherin in the normal endometrium of control patients and the eutopic endometrium of endometriotic patients.
- However, T-cadherin was significantly decreased in the ectopic endometrium of endometriotic patients, compared with control endometrium and eutopic endometrium of endometriosis patients.
Qinsheng Lu and associates from Guangzhou Medical University, China made a unique study of T-cadherin expression in endometriosis and published their results in the journal "Human Reproduction".
Endometriosis is a common condition of reproductive age women, where hormones, immunity, environment and genetic/epigenetic gene alterations play a role in the pathogenesis.
Though endometriosis is not a malignant disease endometriotic tissues have many cancer-like features, such as cell invasion, migration, proliferation, and anti-apoptosis. T-cadherin expression is reduced in various types of cancers, including bladder cancer, lymphoma, prostate cancer, and oral squamous cell carcinomas.
Here, the expression status of T-cadherin in endometriosis and the effects of T-cadherin on migration and invasion of endometrial stromal cells were investigated. The expression status of T-cadherin in 40 patients with and 24 without endometriosis were analyzed. Besides, invasion, migration and signaling pathway regulation of T-cadherin overexpression were studied on isolated endometrial stromal cells.
The expression of T-cadherin was examined by immunohistochemistry staining and western blot. H-score was used to evaluate the staining intensity of T-cadherin. The correlation between T-cadherin expression levels and endometriosis patients’ age, stage, lesion size, and adhesion were analyzed. Endometrial stromal cells were also isolated and cell invasion, migration was detected by transwell assays after T-cadherin overexpression. The expression of vimentin in T-cadherin-overexpressed cells was detected by western blot.
In the current research, there was no difference in the expression of T-cadherin between eutopic endometrium from endometriosis patients versus controls. However, T-cadherin was significantly downregulated in the ectopic endometrium of endometriotic patients, compared with others. T-cadherin is a tumor suppressor in malignancies, so the downregulation of T-cadherin in endometriotic ectopic lesions may play a role in the pathogenesis of endometriosis.
These data presented here provide new insights into the pathogenesis of endometriosis, and T-cadherin may be a new potential therapeutic target also. However, detailed effects and mechanisms of T-cadherin in endometriosis needs to be further studied .