Estradiol promotes EMT in endometriosis via MALAT1/miR200s sponge function

Yu Du, Zhibing Zhang, Wenqian Xiong, Na Li, Hengwei Liu, Haitang He, Qi Li, Yi Liu, Ling Zhang
Reproduction (Cambridge, England) · 2018 · vol. 157(2) , pp. 179–188 · doi:10.1530/rep-18-0424 · PMID:30500775 · W2903330742
article OA: green CC0 ⤵ 51 in-corpus citations
🔓 Open OA copy View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Estradiol upregulates MALAT1 and downregulates miR200s, promoting epithelial-mesenchymal transition (EMT) in endometriosis via a MALAT1/miR200s sponge mechanism.

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

Abstract

Endometriosis is an estrogen-dependent benign gynecological disease that shares some common features of malignancy. Epithelial-mesenchymal transition (EMT) has been recognized as a core mechanism of endometriosis. MALAT1 is widely known as EMT promoter, while miR200 family members (miR200s) are considered as EMT inhibitors. Previous studies have reported that MALAT1 upregulation and miR200s downregulation are observed in endometriosis. MiR200c has been regarded as the strongest member of miR200s to interact with MALAT1. However, whether MALAT1/miR200c regulates EMT remains largely unclear. In this study, the roles of miR200s and MALAT1 in ectopic endometrium were investigated. Additionally, the effects of E2 on EMT and MALAT1/miR200s were examined in both EECs and Ishikawa cells. Notably, E2 could upregulate MALAT1 and downregulate miR200s expression levels and induce EMT in EECs and Ishikawa cells. PHTPP, an ERβ antagonist, could reverse the effect of E2. Overexpression of miR200c and knockdown of MALAT1 significantly inhibited E2-mediated EMT, suggesting that both miR200c and MALAT1 are involved in the E2-induced EMT process in endometriosis. In addition, a reciprocal inhibition was found between miR200s and MALAT1. Therefore, the role of MALAT1/miR200c in EMT is influenced by the presence of estrogen during endometriosis development.

My notes (saved in your browser only)

Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Epithelial-Mesenchymal Transition Estradiol MicroRNAs Peritoneal Diseases Peritoneal Diseases Peritoneal Diseases RNA, Long Noncoding Adult Case-Control Studies Cells, Cultured Epithelial-Mesenchymal Transition Epithelial-Mesenchymal Transition Estradiol Female Gene Expression Regulation Gene Expression Regulation Humans

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 (28)

Cited by (50)

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: 2026-05-13T22:19:25.021412+00:00
License: CC0 · commercial use OK