Targeting hypoxia‐mediated YAP1 nuclear translocation ameliorates pathogenesis of endometriosis without compromising maternal fertility

Shih‐Chieh Lin, Hsiu-Chi Lee, Pei‐Chi Hou, Pei-Chi Hou, Jhao-Lin Fu, Meng-Hsing Wu, Meng‐Hsing Wu, Shaw-Jenq Tsai, Shaw‐Jenq Tsai
The Journal of Pathology · 2017 · vol. 242(4) , pp. 476–487 · doi:10.1002/path.4922 · PMID:28608501 · W2625527931
article OA: closed CC0 ⤵ 12 in-corpus citations
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This study identifies hypoxia-induced YAP1 nuclear translocation as a key driver of endometriosis pathogenesis and demonstrates that inhibiting YAP1 can regress lesions without compromising fertility.

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Abstract

Endometriosis is a highly prevalent gynaecological disease that severely reduces women's health and quality of life. Ectopic endometriotic lesions have evolved mechanisms to survive in the hypoxic peritoneal microenvironment by regulating the expression of a significant subset of genes. However, the master regulator controlling these genes remains to be characterized. Herein, by using bioinformatics analysis and experimental verification, we identified yes-associated protein 1 (YAP1) as a master regulator of endometriosis. Nuclear localization and transcriptional activity of YAP1 were up-regulated by hypoxia via down-regulation of LATS1, a kinase that inactivates YAP1. Disruption of hypoxia-induced YAP1 signalling by siRNA knockdown or inhibitor treatment abolished critical biological processes involved in endometriosis development such as steroidogenesis, angiogenesis, inflammation, migration, innervation, and cell proliferation. Treatment with a YAP1 inhibitor caused the regression of endometriotic lesions without affecting maternal fertility or the growth rate of offspring in the mouse model of endometriosis. Taken together, we identify hypoxia/LATS1/YAP1 as a novel pathway for the pathogenesis of endometriosis and demonstrate that targeting YAP1 might be an alternative approach to treat endometriosis. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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Condition tags

endometriosis

MeSH descriptors

Adaptor Proteins, Signal Transducing Endometriosis Fertility Phosphoproteins Adaptor Proteins, Signal Transducing Adaptor Proteins, Signal Transducing Adaptor Proteins, Signal Transducing Adaptor Proteins, Signal Transducing Animals Cell Cycle Proteins Cell Hypoxia Cell Hypoxia Cell Hypoxia Computational Biology Computational Biology Disease Models, Animal Drug Evaluation, Preclinical Drug Evaluation, Preclinical Endometriosis Endometriosis

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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