Endometriosis is a benign chronic gynecologic condition that develops as a consequence of endometrium (inner lining of the uterus) cells that normally grow inside the uterus initiating their growth outside of the uterus, leading to infertility and pelvic pain, usually during menstruation. It affects as much as 10-15% of all reproductive-age women and the inflammation associated with the cyclic detachment of cells from the wrong site during menstruation is deemed to cause the pain associated with the condition.
Previous studies have shown that very rarely endometriosis cells can transform into cancer cells. Moreover, endometriosis shares some characteristics with cancer as endometriosis cells can invade adjacent organs or even spread (metastasize) to distant organs causing pain localized to those sites. In cancer, these processes are characterized by cancer cells acquiring the ability to penetrate walls of lymphatic and/or blood vessels, after which they circulate to other sites and tissues of the body. Nevertheless, the mechanisms behind such invasion and metastasis processes are not fully understood.
A new study titled “The involvement of osteopontin and matrix metalloproteinase- 9 in the migration of endometrial epithelial cells in patients with endometriosis“, and published in Reproductive Biology and Endocrinology journal tried to evaluate if some of the biological proteins involved in cancer invasion and metastasis are also implicated in endometriosis’ similar behaviors. Specifically, researchers from Ningxia Medical University, China, looked into the role of two proteins known to be responsible for cancer spread, osteopontin (OPN) and matrix metalloproteinase-9 (MMP-9), in endometriotic cell migration.
The team of investigators led by Dr. Mei Yang inhibited the production of OPN and MMP-9 in endometriotic cells using modern molecular biology methods (RNA interference) and activated endometriotic cells, providing estrogen hormone and increasing the production of OPN and MMP-9. As expected, the migration ability of these cells was enhanced upon estrogen treatment. Conversely, these abilities were not augmented in normal endometrial (not-endometriotic) cells.
In the end, these results show that various treatment conditions can affect the production of OPN and MMP-9 in endometriosis. Furthermore, the production of these proteins may be linked to endometriosis’ capacity of invasion and spread to distant organs. Although further research is needed, such basic principles might be used in future research of novel therapeutic agents for endometriosis that can inhibit the migration capacity of these cells and hopefully help with disease management.
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