A high level of TGF-B1 promotes endometriosis development via cell migration, adhesiveness, colonization, and invasiveness†

Upendra Kumar Soni, Sangappa Basanna Chadchan, Sangappa B. Chadchan, Vijay Kumar, Vaibhave Ubba, Mohammad Tariq Ali Khan, Budai Shanmukha Vivek Vinod, Budai S. Vivek Vinod, Rituraj Konwar, Himangsu K. Bora, Himangsu Kousik Bora, Srikanta Kumar Rath, Sharad Sharma, Rajesh Kumar Jha
Biology of reproduction · 2018 · vol. 100(4) , pp. 917–938 · doi:10.1093/biolre/ioy242 · PMID:30423016 · W2901604901
article OA: closed CC0 ⤵ 60 in-corpus citations
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

High levels of TGF-B1 promote endometriosis development in mice by increasing ectopic tissue growth, adhesion, invasiveness, and migration via SMAD2/3, PTEN, integrins, FAK, EMT, and RHOGTPase signaling.

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

Abstract

Endometriosis is a prevalent gynecological disorder that eventually gives rise to painful invasive lesions. Increased levels of transforming growth factor-beta 1 (TGF-B1) have been reported in endometriosis. However, details of the effects of high TGF-B1 on downstream signaling in ectopic endometrial tissue remain obscure. We induced endometriotic lesions in mice by surgical auto-transplantation of endometrial tissues to the peritoneal regions. We then treated endometriotic (ectopic and eutopic endometrial tissues) and nonendometriotic (only eutopic endometrial tissues) animal groups with either active TGF-B1 or PBS. Our results demonstrate that externally supplemented TGF-B1 increases the growth of ectopically implanted endometrial tissues in mice, possibly via SMAD2/3 activation and PTEN suppression. Adhesion molecules integrins (beta3 and beta8) and FAK were upregulated in the ectopic endometrial tissue when TGF-B1 was administered. Phosphorylated E-cadherin, N-cadherin, and vimentin were enhanced in the ectopic endometrial tissue in the presence of TGF-B1 in the mouse model, and correlated with epithelial-mesenchymal transition (EMT) in ovarian endometriotic cells of human origin. Furthermore, in response to TGF-B1, the expression of RHOGTPases (RAC1, RHOC, and RHOG) was increased in the human endometriotic cells (ovarian cyst derived cells from endometriosis patient) and tissues from the mouse model of endometriosis (ectopic endometrial tissue). TGF-B1 enhanced the migratory, invasive, and colonizing potential of human endometriotic cells. Therefore, we conclude that TGF-B1 potentiates the adhesion of ectopic endometrial cells/tissues in the peritoneal region by enhancing the integrin and FAK signaling axis, and also migration via cadherin-mediated EMT and RHOGTPase signaling cascades.

My notes (saved in your browser only)

Condition tags

mesh:D004715endometriosis

MeSH descriptors

Cell Adhesion Cell Movement Endometriosis Peritoneal Diseases Transforming Growth Factor beta1 Adhesiveness Adhesiveness Animals Case-Control Studies Cell Adhesion Cell Movement Cells, Cultured Disease Models, Animal Disease Progression Dose-Response Relationship, Drug Endometriosis Endometriosis Epithelial-Mesenchymal Transition Epithelial-Mesenchymal Transition 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.

References (100)

Cited by (50)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:19:25.021412+00:00
License: CC0 · commercial use OK