ArticleBiology of reproduction2018
Pharmacological blockage of the CXCR4-CXCL12 axis in endometriosis leads to contrasting effects in proliferation, migration, and invasion.
Article in Biology of reproduction, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Inflammatory Changes after Medical Suppression of Suspected Endometriosis for Implantation Failure: Preliminary Results.International journal of molecular sciences · 2024Trial
- Dysregulation of Key Biological Processes in Endometriosis Pathophysiology.Current molecular medicine · 2026Review
- Computational identification of natural CXCR4-binding candidates relevant to endometriosis and ovarian cancer progression.PloS one · 2026Article
- Targeting steroid receptor coactivators for the treatment of benign female reproductive disorders.Endocrine connections · 2025Review
- The role of the CXC chemokine family in endometriosis research and its therapeutic potential.Journal of molecular histology · 2025Review
- Dual targeting of CXCR4 and EZH2 in endometriosis.iScience · 2025Article
- Modelling Endometriosis Using In Vitro and In Vivo Systems.International journal of molecular sciences · 2025Review
- The mechanopathology of the tumor microenvironment: detection techniques, molecular mechanisms and therapeutic opportunities.Frontiers in cell and developmental biology · 2025Review
- Apolipoprotein-B mRNA-editing complex 3B could be a new potential therapeutic target in endometriosis.Scientific reports · 2024Article
- Diagnostic and therapeutic approaches for endometriosis: a patent landscape.Archives of gynecology and obstetrics · 2024Review
- The Effect of Circulating Inflammatory Proteins on Endometriosis: A Mendelian Randomization Study.ImmunoTargets and therapy · 2024Article
- Molecular Mechanisms of Endometriosis Revealed Using Omics Data.Biomedicines · 2023Review
- Oxidative phosphorylation inhibitors inhibit proliferation of endometriosis cells.Reproduction (Cambridge, England) · 2023Article
- Unraveling immunotherapeutic targets for endometriosis: a transcriptomic and single-cell analysis.Frontiers in immunology · 2023Article
- Dissecting theBiomedicines · 2022Article
- Inhibition of METTL3/m6A/miR126 promotes the migration and invasion of endometrial stromal cells in endometriosis†.Biology of reproduction · 2021Article
- CXCR4 protects bone marrow-derived endothelial progenitor cells against hypoxia through the PI3K/Akt signaling pathway.Experimental and therapeutic medicine · 2021Article
- Loss of Cxcr4 in Endometriosis Reduces Proliferation and Lesion Number while Increasing Intraepithelial Lymphocyte Infiltration.The American journal of pathology · 2021Article
- Inflammatory Mediators and Pain in Endometriosis: A Systematic Review.Biomedicines · 2021Review
- Iron-Storage Protein Ferritin Is Upregulated in Endometriosis and Iron Overload Contributes to a Migratory Phenotype.Biomedicines · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
High levels of inflammatory factors including chemokines have been reported in peritoneal fluid and blood of women with endometriosis. CXCL12 mediates its action by interaction with its specific receptor, CXCR4, reported to be elevated in human endometriosis lesions and in the rat model of endometriosis. Activation of the CXCR4-CXCL12 axis increases cell proliferation, migration, and invasion of cancer cells. To obtain insights into the CXCR4 expression profile in lesions and endometrium, as well as functionality of the CXCR4-CXCL12 axis in endometriosis, we analyzed the expression of CXCR4 in tissues on a human tissue array and studied CXCL12-mediated activation of proliferation, invasion, and migration in vitro. We observed differences in levels of nuclear CXCR4 expression among lesion types, being higher in ovarian lesions. Endometriotic cell lines (12Z) showed higher levels of CXCR4, proliferative and migratory potential, and AKT phosphorylation/kinase activity compared to untreated control cells (endometrial epithelial cells). CXCL12 and endometriotic stromal cell-enriched media increased proliferation of non-endometriotic epithelial cells. CXCL12 caused a significant increase in 12Z cell invasion but had no effect on migration; AMD3100, a CXCR4-specific inhibitor, significantly increased invasion of 12Z cells but decreased their migration. However, treatment with CXCL12 plus AMD3100 significantly decreased invasion and migration of 12Z cells. In conclusion, the CXCR4-CXCL12 axis is functional in endometriosis cells, but the expression of CXCR4 varies among lesions. CXCL12 promoted proliferation, migration, and invasion of endometriotic cells, while inducing AKT phosphorylation and activity, but pharmacologically blocking this axis in the absence of the ligand induced their invasiveness.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.