In Endometriosis Study, Enzyme Found to Regulate Hormone-Dependent Migration of Cells

In Endometriosis Study, Enzyme Found to Regulate Hormone-Dependent Migration of Cells

The enzyme phosphatase of regenerating liver-3 (PRL-3) was identified as a key regulator of endometrial stromal cells’ (ESCs) migration in endometriosis. The study, “PRL-3 Is Involved in Estrogen- and IL-6–Induced Migration of Endometrial Stromal Cells From Ectopic Endometrium,” was published in the journal Reproductive Sciences.

PRL-3 overexpression has been found in several cancers, including colorectal cancer, gastric cancer, liver cancer, and lung cancer, leading researchers to propose it as a potential biomarker to determine both tumor aggressiveness and predict outcomes of tumor therapy.

Studies had previously observed a correlation between the expression of PRL-3 and clinical stages and recurrence of endometriosis. Now, researchers investigated the role of PRL-3 in the 17β-estradiol and interleukin 6 (IL-6)-induced migration of endometrial stromal cells (ESCs) from ectopic endometrium.

The team analyzed ectopic endometrial tissues collected from patients with endometriosis for the expression of PRL-3 in both ectopic and eutopic endometrium. They found that PRL-3 was highly expressed in both endometrial glandular cells (EGCs) and ESCs in the ectopic endometrium.

In comparison, researchers found in the eutopic endometrium a weak expression of PRL-3, which was restricted to EGCs. These results suggest PRL-3 may be involved in mediating the development of endometriosis.

Since 17β-estradiol and progesterone are two critical factors contributing to the development and progression of endometriosis, authors hypothesized a potential interaction between these factors and PRL-3 during endometriosis.

They isolated ESCs from ectopic endometrium, which were subsequently treated with 17β-estradiol or progesterone: They found that 17β-estradiol treatment upregulated PRL-3 expression, while progesterone downregulated it.

Moreover, IL-6 treatment alone or combined with 17β-estradiol also increased PRL-3 expression. When treated with an IL-6 antibody, the enhanced PRL-3 expression in ESCs from ectopic endometrium induced by 17β-estradiol treatment was completely reversed.

The team also found that treatment with 17β-estradiol alone and combined with IL-6 led to a significant increase in the migratory capacity of ESCs isolated from ectopic endometrium, which was dependent on PRL-3, since treatment with a PRL-3 inhibitor (sodium orthovanadate) completely abrogated migration.

These results suggest that PRL-3 plays a key role in the 17β-estradiol — and IL-6-induced migration of ESCs from ectopic endometrium.

Patricia holds her Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She also served as a PhD student research assistant in the Laboratory of Doctor David A. Fidock, Department of Microbiology & Immunology, Columbia University, New York.
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Patricia holds her Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She also served as a PhD student research assistant in the Laboratory of Doctor David A. Fidock, Department of Microbiology & Immunology, Columbia University, New York.
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