Tissue Transglutaminase (TG2) as a Candidate Biomarker and Potential Therapeutic Target in Endometriosis: Functional Evidence from shRNA-Mediated Downregulation of TG2 in Endometrial Mesenchymal Stem Cells

İnci Kurt Celep, Melike Batukan, Fikrettin Şahi̇n, Dilek Telci
In: Pharmaceuticals · 2026 · vol. 19(10) , pp. 1520 · doi:10.3390/ph19101520 · W7214276267
Lab / animal OA: gold CC0
🔓 Open OA copy View on OpenAlex View at publisher
⚙ AI-generated summary by qwen3.7-flash, 2026-10-09 ⓘ

Downregulating tissue transglutaminase (TG2) in endometriosis patient-derived mesenchymal stem cells reduces proliferation, migration, and invasion by normalizing matrix metalloproteinase activity, identifying TG2 as a potential diagnostic marker and therapeutic target for the disease.

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

Abstract

Background/Objectives: Endometriosis involves the presence of endometrial tissue outside the uterus. Since the migration of endometrial cells is pivotal to lesion development, tissue transglutaminase (TG2)—known for its roles in cell adhesion, migration, and stemness—may play a significant role. This study aimed to investigate the involvement of TG2 in the migratory and invasive characteristics of endometrial mesenchymal stem cells (eMSCs) derived from healthy individuals and endometriosis patients. Methods: eMSCs were isolated from healthy controls (heMSCs) and endometriosis patients (peMSCs). TG2 protein expression and enzyme activity were evaluated. Co-immunoprecipitation (Co-IP) experiments were performed to assess TG2 associations with ITGβ-1 and SDC-4 in membrane fractions. Additionally, shRNA technology was utilized to silence TG2 in peMSCs to analyze its effects on cell proliferation, migration, invasion, and matrix metalloproteinase (MMP-2 and -9) activities. Results: peMSCs exhibited higher TG2 protein expression but lower enzyme activity compared to heMSCs. Co-IP analysis of membrane fractions revealed enhanced association of TG2 with ITGβ-1 and SDC-4 in peMSCs, thereby promoting enhanced cell survival, migration, and invasive properties. Silencing TG2 in peMSCs via shRNA eliminated these enhanced proliferation, migration, and invasion capabilities, reverting them to a phenotype resembling heMSCs. Furthermore, elevated MMP-2 and -9 activities returned to basal levels following TG2 knockdown. Conclusions: These findings suggest that TG2 acts as a distinctive cell adhesion molecule directly involved in endometriosis pathogenesis. Collectively, these findings identify TG2 as a disease-associated molecular marker warranting further evaluation for its diagnostic potential and suggest that targeting its cell-adhesion functions may represent a novel therapeutic strategy for endometriosis.

My notes (saved in your browser only)

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 (55)

Source provenance

openalex
last seen: 2026-10-14T06:01:35.214979+00:00
License: CC0 · commercial use OK