A new hope for a "targeted" drug for endometriosis

A new hope for a

Membrane receptors are responsible for the adhesive ability of endometriotic stromal cells.

Key Points


  • Targeted drugs against ANTRX2(anthrax toxin receptor 2) decrease adhesion, progression, and angiogenesis of endometriotic lesions in-vitro,and in mouse models in-vivo.


  • Elevated levels of ANTRX2, one of the membrane receptors, is expressed in endometriotic cells,  promotes proliferation, adhesion, and induce angiogenesis.
  • Increased levels of ANTRX2 activates the factors that promote cell proliferation and angiogenesis while blocking ANTXR2 signaling by siRNA prevents mouse endometriotic lesion formation. 
  • ANTRX2 targeted drugs may be used for endometriosis therapy.

What's done here:

  • The authors planned prospective, controlled in-vitro and in-vivo research to examine the role of membrane receptor ANTRX2 on endometriosis proliferation and adhesion.

Key results:

  • In-vitro endometriotic specimens showed upregulation of ANTRX2 provoked by hypoxia.  
  • When compared with normal endometrium, ANTRX2 expression is elevated in ectopic endometriotic stromal cells.
  • In the mouse model, endometriosis formation reduced by pharmacologically blocking ANTRX2 mediated signaling.


In spite of carefully designed research, laboratory technics, and statistical care, study groups in this research are restricted to declare inventions on endometriosis progression.

Lay Summary

Lin et al. from National Cheng Kung University, Taiwan, recently published in"Theranostics" the article entitled "Targeting Anthrax Toxin Receptor 2 Ameliorates Endometriosis Progression”,  report that ANTRX2 may be a novel therapeutic target for endometriosis.

Thinking that the adhesion should be the first and the most critical step for retrogradely transferred endometrial tissues to develop endometriosis, authors tried to identify novel and druggable targets involved in the adhesion of endometriotic lesions. In this prospective study, they identified that ANTXR2, a membrane receptor, is overexpressed in ectopic endometriotic cells by using bioinformatics and molecular approaches.

The authors first searched public databases and selected ANTRX2 (anthrax toxin receptor 2) to study because it is a major virulent factor responsible for the entry of anthrax toxin into the cell. To reveal the overexpression of ANTHX2 receptors in endometriotic patients, the researchers examined the eutopic and ectopic endometrial tissues obtained from laparoscopy and laparotomy patients of Obstetrics and Gynecology Department of Cheng Kung University by a variety of in-vitro assays.

After verifying ANTRX2 is upregulated both in eutopic and ectopic endometriotic cells, researchers isolated stromal cells from the of endometriosis tissues and realized that the aberrant expression of ANTXR2 was induced by hypoxia-mediated epigenetic regulation of histone modification.

They also clarified the signaling cascade and pathological functions of ANTXR2, and more importantly, the authors demonstrated by in-vivo research in a mouse model that pharmacological blockage of ANTXR2-mediated signaling, endometriosis development was prevented and the established endometriotic lesions regressed.

"Higher ANTXR2 level contributes to an increased adhesive ability of endometriotic stromal cells. More importantly, we show, for the first time, that ANTXR2 activates Yes-Associated Protein 1, a transcription activator that promotes cell proliferation and angiogenesis while blocking ANTXR2 signaling prevents mouse endometriotic lesion formation. Taken together, our current findings provide solid evidence to demonstrate that disrupting aberrant cellular adhesive ability may represent an alternative approach to treat endometriosis" concluded the authors.

Collecting all inventions together, they claimed using targeted drugs for ANTRX2 can cure adhesion, progression, and angiogenesis of endometriotic lesions.



Research Source: https://www.ncbi.nlm.nih.gov/pubmed/30809297

membrane receptors eutopic endometrial cells cell adhesion hypoxia ANTXR2 EZH2 endometriosis


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