Role of SMOC2 in adenomyosis: implications for ECM remodeling and EMT pathogenesis

Lihui Wang, Lei-Na Wang, Li Ren, Lin Li, Shu-Lian Liu, Shuangjuan Liu, Haoda Lu, Hua-Jie Lu, Meng-Lan Guo, Ming Guo, Xiao-Min Niu, Xiaomin Niu, Shiwali Vinita, Shuang Ning, Shuluo Ning, Li-Ping Han, Liping Han
BMC women's health · 2025 · vol. 25(1) , pp. 155 · doi:10.1186/s12905-025-03700-8 · PMID:40181364 · W4409168238
article OA: gold CC0 ⤵ 2 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study found that higher SMOC2 expression in adenomyosis promotes extracellular matrix remodeling and epithelial-mesenchymal transition, suggesting SMOC2 as a potential therapeutic target for the disease.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This study examined whether SMOC2, an extracellular matrix-associated protein, is differentially expressed in adenomyosis and whether it regulates extracellular matrix remodeling and epithelial–mesenchymal transition (EMT). Using ectopic endometrial tissue from 35 adenomyosis patients and control endometrium from 30 women, the authors performed immunohistochemistry and Masson staining, and used primary cell culture with CCK-8, real-time PCR, and western blotting to test SMOC2 effects on proliferation and EMT markers. SMOC2 was significantly higher in adenomyosis ectopic tissue, promoted cell proliferation, upregulated mesenchymal markers (N-cadherin, α-SMA) while downregulating epithelial marker E-cadherin, and activated the MMP9 signaling pathway implicated in ECM remodeling; SMOC2 knockdown with siRNA reversed these changes, though the paper’s tissue sample availability and functional work were limited by clinical specimen sourcing. This paper is centrally about endometriosis—its title and background position SMOC2 as an ECM-associated driver of EMT and ECM remodeling in ectopic lesions, with adenomyosis as the specific experimental focus.

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Abstract

BACKGROUND: Adenomyosis is a common gynecological disorder characterized by the invasion of endometrial tissue into the myometrium, resulting in severe dysmenorrhea and menorrhagia. This study aimed to explore the role of SMOC2 (SPARC related modular calcium binding 2), an extracellular matrix (ECM) -associated protein, in the pathogenesis of adenomyosis and its potential as a therapeutic target. METHODS: We conducted a clinical study involving 35 patients diagnosed with adenomyosis and 30 controls. Ectopic endometrial tissue samples were collected and analyzed using immunohistochemistry (IHC), Masson staining, and cell culture techniques. The proliferative effect of SMOC2 on cells was evaluated using CCK- 8 assay, while the expression of SMOC2 and epithelial-mesenchymal transition (EMT) was assessed using real-time PCR and western blot analysis. RESULTS: SMOC2 expression was significantly higher in the ectopic endometrial tissue of adenomyosis patients compared to controls. SMOC2 could promote cell proliferation. Overexpression of SMOC2 significantly upregulated mesenchymal markers N-cadherin and α-SMA, and downregulated epithelial marker E-cadherin. Conversely, knocking down SMOC2 with siRNA reversed these effects. These findings indicate that SMOC2 promotes EMT in adenomyotic stromal cells. Additionally, SMOC2 also activated the MMP9 signaling pathway, which plays a crucial role in the extracellular matrix (ECM) remodeling. CONCLUSIONS: SMOC2 appears to be a key regulator in the pathogenesis of adenomyosis, promoting ECM remodeling and EMT, both of which are characteristic of the disease. Targeting SMOC2 may provide a novel therapeutic strategy for the treatment of adenomyosis.

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Condition tags

adenomyosisdysmenorrhea

MeSH descriptors

Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Calcium-Binding Proteins Calcium-Binding Proteins Calcium-Binding Proteins Calcium-Binding Proteins Calcium-Binding Proteins Calcium-Binding Proteins Calcium-Binding Proteins Calcium-Binding Proteins Calcium-Binding Proteins Epithelial-Mesenchymal Transition

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.

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