Activated Hippo/Yes-Associated Protein Pathway Promotes Cell Proliferation and Anti-apoptosis in Endometrial Stromal Cells of Endometriosis

Yong Song, Jing Fu, Min Zhou, Li Xiao, Xue Feng, Hengxi Chen, Wei Huang, Tingting Liu
The Journal of clinical endocrinology and metabolism · 2016 · vol. 101(4) , pp. 1552–1561 · doi:10.1210/jc.2016-1120 · PMID:26977530 · W2301845119
article OA: bronze CC0 ⤵ 46 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

The Hippo/YAP pathway is activated in endometriosis, promoting cell proliferation and inhibiting apoptosis by upregulating TEAD1, CTGF, and BCL-2.

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

Abstract

CONTEXT: The imbalance in cell proliferation and apoptosis is considered an important role in the pathogenesis of endometriosis, but the exact mechanisms remains unclear. A newly established signaling pathway–Hippo/Yes-associated protein (YAP) pathway plays a critical role in the proliferation and apoptosis processes. However, studies focusing on Hippo/YAP pathway and endometriosis are lacking. OBJECTIVE: The objective was to explore the function of the Hippo/YAP pathway in endometriosis. SETTING AND DESIGN: The expression of YAP was first investigated in endometrium of women with or without endometriosis. The role of YAP in cell proliferation and apoptosis is identified by transfection of endometrial stromal cells (ESCs) in vitro, subsequent Verteporfin treatments in eutopic ESCs in vitro, and endometriosis animal model of nude mice in vivo. RESULTS: Our results revealed that increased expression of YAP and decreased expression of p-YAP in ectopic and eutopic endometrium compared with normal endometrium. YAP knockdown in eutopic ESCs decreased cell proliferation and enhanced cell apoptosis companied with decreased expression of TEAD1, CTGF, and B-cell lymphoma/leukemia (BCL)-2; whereas overexpression of YAP resulted in increased proliferation and decreased apoptosis of normal ESCs with increased expression of TEAD1, CTGF, and BCL-2. By chromatin immunoprecipitation qPCR CTGF and BCL-2 were identified as directly downstream target genes of YAP-TEAD1 active complex. Eutopic ESCs treated with Verteporfin revealed decreased proliferation and enhanced apoptosis whereas in endometriosis animal models of nude mice treated with Verteporfin, the size of endometriotic lesions was significantly reduced. CONCLUSIONS: Our study suggests that the Hippo/YAP-signaling pathway plays a critical role in the pathogenesis of endometriosis and should present a novel therapeutic method against endometriosis.

My notes (saved in your browser only)

Condition tags

mesh:D004715endometriosis

MeSH descriptors

Apoptosis Cell Proliferation Endometriosis Endometrium Protein Serine-Threonine Kinases Proto-Oncogene Proteins c-yes Stromal Cells Adult Animals Blotting, Western Endometriosis Endometriosis Endometriosis Endometrium Endometrium Female Flow Cytometry Hippo Signaling Pathway Humans Immunoenzyme Techniques

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 (31)

Cited by (46)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-04T00:00:01.174412+00:00
pubmed
last seen: 2026-05-13T22:21:13.485820+00:00
License: CC0 · commercial use OK