ArticleReproduction (Cambridge, England)2019
Estradiol promotes EMT in endometriosis via MALAT1/miR200s sponge function.
Article in Reproduction (Cambridge, England), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 75 citations in OpenAlex.
- Estradiol alters actin and protrusion dynamics in endometriotic epithelial cells.Journal of biological physics · 2026Article
- Looking at endometriosis-diagnosis and disease mechanisms through a mechanical lens.Frontiers in medicine · 2026Review
- Long noncoding RNAs and microRNAs in Endometriosis.Biomedicines · 2025Review
- Insights into the Molecular Mechanisms and Signaling Pathways of Epithelial to Mesenchymal Transition (EMT) in the Pathophysiology of Endometriosis.International journal of molecular sciences · 2025Review
- Potential Regulation of the Long Non-Coding RNA Metastasis-Associated Lung Adenocarcinoma Transcript1 by Estrogen in Parkinson's Disease.Life (Basel, Switzerland) · 2024Review
- Review
- Impaired bone morphogenetic protein (BMP) signaling pathways disrupt decidualization in endometriosis.Communications biology · 2024Article
- Potential roles of lncRNA MALAT1-miRNA interactions in ocular diseases.Journal of cell communication and signaling · 2023Review
- Impaired bone morphogenetic protein (BMP) signaling pathways disrupt decidualization in endometriosis.Research square · 2023Article
- Linc-ROR Promotes EMT by Targeting miR-204-5p/SMAD4 in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- Review
- Spheroids as a model for endometriotic lesions.JCI insight · 2023Article
- The Critical Roles of Circular RNAs in Basic Research and Clinical Application of Female Reproductive-Related Diseases.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- A comprehensive overview of exosome lncRNAs: emerging biomarkers and potential therapeutics in endometriosis.Frontiers in endocrinology · 2023Review
- LncRNA-miRNA-mRNA regulatory axes in endometrial cancer: a comprehensive overview.Archives of gynecology and obstetrics · 2022Review
- Single Cell Sequencing Reveals Mechanisms of Persistent Truncus Arteriosus Formation afterGenes · 2022Article
- Epithelial-mesenchymal transition process during embryo implantation.Cell and tissue research · 2022Review
- Molecular Signatures Correlated With Poor IVF Outcomes: Insights From the mRNA and lncRNA Expression of Endometriotic Granulosa Cells.Frontiers in endocrinology · 2022Article
- Oestrogen-induced epithelial-mesenchymal transition (EMT) in endometriosis: Aetiology of vaginal agenesis in Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome.Frontiers in physiology · 2022Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.