Decoy receptor 3 promotes cell adhesion and enhances endometriosis development

Hsiao-Wen Tsai, Hsiao‐Wen Tsai, Ming-Ting Huang, Huang MT, Ming‐Ting Huang, Wang PH, Peng‐Hui Wang, Peng-Hui Wang, Ben-Shian Huang, Ben‐Shian Huang, Huang BS, Chen YJ, Yi-Jen Chen, Yi‐Jen Chen, Shie-Liang Hsieh, Shie‐Liang Hsieh
The Journal of Pathology · 2017 · vol. 244(2) , pp. 189–202 · doi:10.1002/path.5000 · PMID:29057478 · W2786939632
article OA: closed CC0 ⤵ 17 in-corpus citations
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-06 ⓘ

Decoy receptor 3 is upregulated in endometriosis, promoting cell adhesion and ectopic endometrial growth via the Akt-NF-κB pathway, with its expression correlating to disease severity.

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

Abstract

Endometriosis is a multifactorial inflammatory disease with persistent activation of the nuclear factor-κB (NF-κB) signalling pathway. Aberrant adhesion of endometrium is the essential step in the progression of endometriosis, but the molecular mechanism of ectopic growth of endometrium is still unclear. Decoy receptor 3 (DcR3)/TNFRSF6B, a pleiotropic immunomodulator regulated by oestrogen, is able to activate focal adhesion kinase to promote cell adhesion. We found that DcR3 is upregulated in human ectopic endometrial cells via activation of the Akt-NF-κB signalling pathway, and its expression level correlates positively with that of the adhesion molecules intercellular adhesion molecule 1 (ICAM-1) and homing cell adhesion molecule (HCAM; CD44). In a multivariate regression model, DcR3 expression level was the most significant parameter associated with endometriosis severity. Knockdown of DcR3 not only downregulated the expression of ICAM-1 and HCAM, but also reduced cell adhesion and migration. In vivo investigation further showed that DcR3 promoted the growth and spread of endometrium, whereas knockdown of DcR3 by lentivirus-delivered short hairpin RNA inhibited ectopic adhesion of endometrium and abrogated endometriosis progression. These observations are in support of DcR3 playing a critical role in the pathogenesis of endometriosis, and the inhibition of DcR3 expression being a promising approach for the treatment of endometriosis. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Cell Adhesion Endometriosis Endometrium Receptors, Tumor Necrosis Factor, Member 6b Animals Case-Control Studies Cell Adhesion Molecules Cell Adhesion Molecules Cell Line, Tumor Cell Movement Disease Models, Animal Disease Progression Endometriosis Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Endometrium

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 (58)

Cited by (19)

Source provenance

europepmc
last seen: 2026-09-15T06:16:59.523076+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:20:13.663096+00:00
unpaywall
last seen: 2026-09-15T06:33:26.365676+00:00
License: CC0 · commercial use OK