Abnormal activation of the Wnt3a/β-catenin signaling pathway promotes the expression of TBX3 and the EMT pathway to mediate the occurrence of adenomyosis

Mengqi Li, Ting Li, Tingting Jin, Yi Chen, Lan Cheng, Qiheng Liang, Simiao Yan, Tingting Li, Wanqun Chen, Qingzhen Ran
In: Research Square · 2023 · doi:10.21203/rs.3.rs-2803345/v1 · W4372348011
preprint OA: green CC0
📄 Open PDF View on OpenAlex View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

Abnormal Wnt3a/β-catenin signaling activates TBX3 and ERα, promoting epithelial-to-mesenchymal transition, cell proliferation, and invasion in a mouse model of adenomyosis.

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, 2026-06-10 ⓘ

This preprint investigated whether the transcription factor TBX3 contributes to adenomyosis and whether TBX3 is regulated by the Wnt3a/β-catenin signaling pathway. Using a tamoxifen-induced ICR mouse adenomyosis model, the authors assessed protein expression (western blotting and immunohistochemistry) and measured proliferation and apoptosis (PCNA and TUNEL), while testing the role of Wnt signaling with the intraperitoneal inhibitor XAV-939. They found TBX3 overexpression and epithelial-to-mesenchymal transition (EMT) in adenomyosis were associated with activation of the Wnt3a/β-catenin pathway, and that XAV-939 reduced TBX3 and EMT, suppressed proliferation, limited endometrial invasion depth, and decreased ERα expression. The paper does not explicitly state a limitation in the provided excerpt, but it is based on an animal model and protein-level assays rather than direct mechanistic confirmation beyond pathway inhibition. This paper is centrally about endometriosis and/or adenomyosis—specifically adenomyosis—because it uses an adenomyosis mouse model to link Wnt3a/β-catenin signaling and TBX3-driven EMT with adenomyosis development.

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

Abstract

Abstract Background TBX3 is a transcription factor that can regulate cell proliferation, apoptosis, invasion, and migration in different tumor cells; however, its role in adenomyosis (ADM) has not been previously studied. Some of ADM’s pathophysiological characteristics are similar to those of malignant tumors (e.g., abnormal proliferation, migration, and invasion). Methods and results we hypothesized that TBX3 might have a role in ADM. We used tamoxifen-induced ICR mice to establish ADM disease model. The study procedure included western blotting and immunohistochemistry to analyze protein levels; additionally, we used intraperitoneal injection of Wnt/β-catenin pathway inhibitor XAV-939 to study the relationship between TBX3 and Wnt/β-catenin pathway as well as PCNA and TUNEL to detect cell proliferation and apoptosis, respectively. TBX3 overexpression and epithelial-to-mesenchymal transition (EMT) in ADM mice was found to be associated with activation of the Wnt3a/β-catenin pathway. Treatment with XAV-939 in ADM mice led to the inhibition of both TBX3 and EMT; moreover, abnormal cell proliferation was suppressed, the depth of invasion of endometrium cells was limited and the expression of ERα was suppressed. Thus, the use of XAV-939 effectively inhibited further invasion of endometrial cells. Conclusion These findings suggest that TBX3 may play an important role in the development of ADM. The expression of TBX3 in ADM was regulated by the Wnt3a/β-catenin pathway. The activation of the Wnt3a/β-catenin pathway in ADM promoted TBX3 and ERα expression and induced the occurrence of EMT, thus promoting cell proliferation and inhibiting apoptosis, ultimately accelerating the development of ADM. The study provides a reference for the diagnosis of ADM

My notes (saved in your browser only)

Condition tags

adenomyosis

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 (45)

Source provenance

europepmc
last seen: 2026-06-11T06:38:44.028908+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0 · commercial use OK