Abstract
Endometriosis a benign gynaecological disease, associated with chronic inflammation and increased levels of chemokines. Lesions are composed of endometrial stroma and glands localized outside the uterus. In a rat model of endometriosis, we showed high CXCR4 mRNA levels in endometriotic lesions and in high protein expression levels in human endometriosis tissues compared to control endometrium . The CXCR4‐CXCL12 axis plays roles in proliferation, migration, and cell invasion. Endometriotic epithelial cells expressed CXCR4. We hypothesized that CXCL12 may induce proliferation, migration, and invasion of endometriotic cells (12Z) compared to a non‐invasive breast cancer cells, expressing endometrial markers (EEC), and the induction may be blocked by the CXCR4 inhibitor, AMD3100. Cell proliferation in response to CXCL12 was analyzed by BrdU assay. We also studied cell invasion and migration in response to CXCL12 and AMD3100 by invasion and migration chambers. Rat model of endometriosis was used to identify the effect of AMD3100 in lesions regression. CXCL12 increased proliferation and migration of EEC, and invasion in 12Z cells, compared to media (p<0.05). AMD3100 reduced migration in EEC; reduced migration and increased invasion in 12Z cells (p<0.05). These data suggest that the CXCR4‐CXCL12 axis can be activated in endometrial cells to promote cell proliferation, migration, and invasion, and application of cancer treatments to endometriosis disease requires additional studies. These biological functions have been previously shown to be dysregulated in endometriosis, by still undefined mechanisms, leading to survival and growth of ectopic endometrium.Grant Funding Source: Supported by F31HD072594, RCMI G12‐MD007579, R25GM082406, R25GM096955, R01‐HD050509
Published Version
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