Promotion of BST2 expression by the transcription factor IRF6 affects the progression of endometriosis

Jixin Li, Yanan He, Yanjun Qu, Cheng-Cheng Ren, Chengcheng Ren, Xiaotong Wang, Yan Cheng, Liyuan Sun, Xin Zhang, Guangmei Zhang
Frontiers in immunology · 2023 · vol. 14 , pp. 1115504 · doi:10.3389/fimmu.2023.1115504 · PMID:37143676 · PMC10151653 · W4366293990
article OA: gold CC0 ⤵ 4 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

The transcription factor IRF6 promotes BST2 expression, which is involved in NF-κB signaling, lymphangiogenesis, and endometriosis progression.

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, 2026-06-08 ⓘ

This study investigated whether BST2 (CD317) contributes to endometriosis progression by examining ectopic versus normal endometrial tissues, cultured stromal cells, and an in vivo mouse endometriosis model, using bioinformatic target identification alongside functional assays, IHC, qRT-PCR, western blotting, and siRNA knockdown. BST2 was significantly upregulated in ectopic endometrial tissues and cells and promoted proliferation, migration, and lymphangiogenesis while inhibiting apoptosis, with results linked to activation of the canonical NF-κB signaling pathway. Mechanistically, the transcription factor IRF6 directly induced BST2 by binding the BST2 promoter, and the authors described a feedback context involving immune-cell infiltration, IL-1β production, and further NF-κB activation to support lymphangiogenesis, while explicitly noting none of the stated limitations in the provided text. This paper is centrally about endometriosis — it identifies an IRF6–BST2 axis that regulates NF-κB signaling and lymphangiogenesis in endometriosis lesions.

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

Abstract

BACKGROUND: Endometriosis (EM) is a benign, multifactorial, immune-mediated inflammatory disease that is characterized by persistent activation of the NF-κB signaling pathway and some features of malignancies, such as proliferation and lymphangiogenesis. To date, the pathogenesis of EM is still unclear. In this study, we investigated whether BST2 plays a role in the development of EM. METHODS: Bioinformatic analysis was performed with data from public databases to identify potential candidate targets for drug treatment. Experiments were conducted at the cell, tissue, and mouse EM model levels to characterize the aberrant expression patterns, molecular mechanisms, biological behaviors of endometriosis as well as treatment outcomes. RESULTS: BST2 was significantly upregulated in ectopic endometrial tissues and cells compared with control samples. Functional studies indicated that BST2 promoted proliferation, migration, and lymphangiogenesis and inhibited apoptosis in vitro and in vivo. The transcription factor (TF) IRF6 induced high BST2 expression by directly binding the BST2 promoter. The underlying mechanism by which BST2 functions in EM was closely related to the canonical NF-κB signaling pathway. New lymphatic vessels may serve as a channel for the infiltration of immune cells into the endometriotic microenvironment; these immune cells further produce the proinflammatory cytokine IL-1β, which in turn further activates the NF-κB pathway to promote lymphangiogenesis in endometriosis. CONCLUSION: Taken together, our findings provide novel insight into the mechanism by which BST2 participates in a feedback loop with the NF-κB signaling pathway and reveal a novel biomarker and potential therapeutic target for endometriosis.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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 (78)

Cited by (4)

Source provenance

europepmc
last seen: 2026-06-13T06:22:48.782012+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-06-13T06:21:50.575914+00:00
License: CC0 · commercial use OK