Targeting EphA2 suppresses the proliferation, migration and invasion of endometriosis via the AMPK signaling pathway

Chaoyi Yang, Shujun Wang, Mengru Li, Xiangli Pang, Aili Tan
European journal of histochemistry : EJH · 2025 · vol. 69(3) · doi:10.4081/ejh.2025.4168 · PMID:40525819 · PMC12210881 · W4411376685
article OA: gold CC0
📄 Open PDF Full text JSON View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Elevated EphA2 expression in endometriosis was targeted to inhibit cell proliferation, migration, and invasion via the AMPK signaling pathway.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

The paper investigated EphA2 expression in endometriosis and the regulatory mechanism by which EphA2 might affect endometriotic stromal cells, using bioinformatics analyses of Eph protein family expression followed by clinical verification (qPCR, Western blot, immunohistochemistry) of EphA2 levels. In vitro experiments using primary eutopic endometriotic stromal cells showed that blocking EphA2 inhibited cell proliferation, migration, and invasion, alongside modulation of the AMPK signaling pathway, and the authors report an association between elevated EphA2 levels and endometriosis patients. A key limitation stated implicitly is that functional outcomes were tested in vitro on primary eutopic endometriotic stromal cells rather than in vivo. This paper is centrally about endometriosis — it tests whether targeting EphA2 suppresses stromal cell proliferation, migration, and invasion through AMPK signaling.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Endometriosis is a benign disease with similar characteristics to tumors. Recent studies have found that the erythropoietin-producing hepatoma receptor A2 (EphA2) has the dual effect of promoting tumor and inhibiting tumor. The objective of this study was to explore the specific regulatory mechanism of EphA2 in endometriosis. The expression level of Eph protein family in endometriosis was analyzed by bioinformatics method. At the clinical level, qPCR, Western blot and immunohistochemistry were used to verify the correlation between increased EphA2 levels and endometriosis. The effects of blocking EphA2 on cell migration, invasion, proliferation and apoptosis of primary eutopic endometriotic stromal cells were explored in vitro. Our study indicated that EphA2 expression was elevated in endometriosis patients, and blocking EphA2 in vitro inhibited cell proliferation, migration and invasion through AMPK signaling pathway. Targeting EphA2 can inhibit the progression of endometriosis through the AMPK signaling pathway.
Full text 1,870 characters · extracted from oa-doi-fallback · click to expand
Targeting EphA2 suppresses the proliferation, migration and invasion of endometriosis via the AMPK signaling pathway All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher. Authors Endometriosis is a benign disease with similar characteristics to tumors. Recent studies have found that the erythropoietin-producing hepatoma receptor A2 (EphA2) has the dual effect of promoting tumor and inhibiting tumor. The objective of this study was to explore the specific regulatory mechanism of EphA2 in endometriosis. The expression level of Eph protein family in endometriosis was analyzed by bioinformatics method. At the clinical level, qPCR, Western blot and immunohistochemistry were used to verify the correlation between increased EphA2 levels and endometriosis. The effects of blocking EphA2 on cell migration, invasion, proliferation and apoptosis of primary eutopic endometriotic stromal cells were explored in vitro. Our study indicated that EphA2 expression was elevated in endometriosis patients, and blocking EphA2 in vitro inhibited cell proliferation, migration and invasion through AMPK signaling pathway. Targeting EphA2 can inhibit the progression of endometriosis through the AMPK signaling pathway. Ethics Approval the clinical study was approved by the Ethics Committee of Renmin Hospital of Wuhan University (clinical trial number: WDRY2024-K111)Supporting Agencies Natural Science Foundation of Hubei Province, National Natural Science Foundation of ChinaHow to Cite This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

⚙ Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback ⓘ

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

endometriosis

MeSH descriptors

AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases AMP-Activated Protein Kinases Cell Movement Cell Movement Cell Movement

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (54)

SciLite annotations

chemicals 24
steroid estrogen progesterone estrogen formaldehyde xylene ethanol ethanol ethanol ethanol water citric acid formaldehyde penicillin streptomycin cu(i)-s-mo(iv)(=o)o-nbic cluster crystal violet water propidium iodide 27-norcholestanehexol cu(i)-s-mo(iv)(=o)o-nbic cluster n-[(2r,3r,4r,5s,6r)-2-[[(2r,3r,4r,5r,6s)-5-acetamido-6-[(2r,3r,4s,5s,6r)-2-[(2r,3r,4r,5r,6s)-4,5-dihydroxy-2-(hydroxymethyl)-6-[(2r,3s,4r,5r,6r)-4,5,6-trihydroxy-2-(hydroxymethyl)oxan-3-yl]oxyoxan-3-yl]oxy-3,5-dihydroxy-6-(hydroxymethyl)oxan-4-yl]oxy-3-hydroxy-4-[(2r,3r,4s,5r,6r)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyoxan-2-yl]methoxy]-4,5-dihydroxy-6-(hydroxymethyl)oxan-3-yl]acetamide n-[(2r,3r,4r,5s,6r)-2-[[(2r,3r,4r,5r,6s)-5-acetamido-6-[(2r,3r,4s,5s,6r)-2-[(2r,3r,4r,5r,6s)-4,5-dihydroxy-2-(hydroxymethyl)-6-[(2r,3s,4r,5r,6r)-4,5,6-trihydroxy-2-(hydroxymethyl)oxan-3-yl]oxyoxan-3-yl]oxy-3,5-dihydroxy-6-(hydroxymethyl)oxan-4-yl]oxy-3-hydroxy-4-[(2r,3r,4s,5r,6r)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyoxan-2-yl]methoxy]-4,5-dihydroxy-6-(hydroxymethyl)oxan-3-yl]acetamide imatinib
organisms 1
rodents

Source provenance

europepmc
last seen: 2026-06-11T06:19:48.454388+00:00
openalex
last seen: 2026-06-04T00:00:01.174412+00:00
pmc
last seen: 2026-05-13T20:22:03.195721+00:00
pubmed
last seen: 2026-05-26T00:31:20.206735+00:00
scilite
last seen: 2026-05-18T04:26:01.642840+00:00
License: CC0 · commercial use OK