ArticleStem cell research & therapy2019
miR-205-5p inhibits human endometriosis progression by targeting ANGPT2 in endometrial stromal cells.
Article in Stem cell research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 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
27 citing papers in PubMed, 41 citations in OpenAlex.
- Advances in the biological functions of miR‑205 in various diseases (Review).Molecular medicine reports · 2026Review
- Endothelial miR-7052 Safeguards Blood-Brain Barrier Integrity During Endotoxemia by Co-repressing ANGPT2 and PDE5A.Molecular neurobiology · 2026Article
- Precision Therapeutic and Preventive Molecular Strategies for Endometriosis-Associated Infertility.International journal of molecular sciences · 2025Review
- Drug Repurposing for Targeting ISL LIM Homeobox 2 in Treatment of Endometriosis: A Computational Study.International journal of fertility & sterility · 2025Article
- miR-450b-5p promotes development of endometriosis by inhibiting the GABPA/HOXD10 axis.iScience · 2024Article
- PDLIM3 knockdown promotes ferroptosis in endometriosis progression via inducing Gli1 degradation and blocking Hedgehog signaling pathway.Journal of assisted reproduction and genetics · 2024Article
- Comparison of cervicovaginal fluid extracellular vesicles isolated from paired cervical brushes and vaginal swabs.Journal of extracellular biology · 2024Article
- The Pathological Role of miRNAs in Endometriosis.Biomedicines · 2023Review
- Nucleocytoplasmic transport of active HER2 causes fractional escape from the DCIS-like state.Nature communications · 2023Article
- Knockdown of miR-27a reduces TGFβ-induced EMT and HAmerican journal of translational research · 2023Article
- LncRNA IGF2-AS promotes endometriosis progression through targeting miR-370-3p/IGF2 axis and activating PI3K/AKT/mTOR signaling pathway.Journal of assisted reproduction and genetics · 2022Article
- Integrated bioinformatic analysis of dysregulated microRNA-mRNA co-expression network in ovarian endometriosis.Acta obstetricia et gynecologica Scandinavica · 2022Article
- HOXB5-activated ANGPT2 promotes the proliferation, migration, invasion and angiogenic effect of esophageal cancer cells via activating ERK/AKT signaling pathway.Experimental and therapeutic medicine · 2022Article
- Roles of microRNAs in Regulating Apoptosis in the Pathogenesis of Endometriosis.Life (Basel, Switzerland) · 2022Review
- Restoration of miR-223-3p expression in aged mouse uteri with Samul-tang administration.Integrative medicine research · 2022Article
- miR-205-5p in exosomes divided from chondrogenic mesenchymal stem cells alleviated rheumatoid arthritis via regulating MDM2 in fibroblast-like synoviocytes.Journal of musculoskeletal & neuronal interactions · 2022Article
- Role of repressed microRNAs in endometriosis.Medical molecular morphology · 2022Review
- hsa-miR-199a-3p Inhibits Motility, Invasiveness, and Contractility of Ovarian Endometriotic Stromal Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- New Therapeutics in Endometriosis: A Review of Hormonal, Non-Hormonal, and Non-Coding RNA Treatments.International journal of molecular sciences · 2021Review
- Role of miRNAs in Normal Endometrium and in Endometrial Disorders: Comprehensive Review.Journal of clinical medicine · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundmiRNA expression profiles in ectopic endometrium (EC) serving as pathophysiologic genetic fingerprints contribute to determining endometriosis progression; however, the underlying molecular mechanisms remain unknown.
methodsmiRNA microarray analysis was used to determine the expression profiling of EC fresh tissues. qRT-PCR was performed to screen miR-205-5p expression in EC tissues. The roles of miR-205-5p and its candidate target gene, angiopoietin-2 (ANGPT2), in endometriosis progression were confirmed on the basis of both in vitro and in vivo systems. miR-205-5p and ANGPT2 expression were measured by in situ hybridization and immunochemistry, and their clinical significance was statistically analysed.
resultsmiR-205-5p was screened as a novel suppressor of endometriosis through primary ectopic endometrial stromal cell migration, invasion, and apoptosis assay in vitro, along with endometrial-like xenograft growth and apoptosis in vivo. In addition, ANGPT2 was identified as a direct target of miR-205-5p through bioinformatic target prediction and luciferase reporter assay. Re-expression and knockdown of ANGPT2 could respectively rescue and simulate the effects induced by miR-205-5p. Importantly, the miR-205-5p-ANGPT2 axis was found to activate the ERK/AKT pathway in endometriosis. Finally, miR-205-5p and ANGPT2 expression were closely correlated with the endometriosis severity.
conclusionThe newly identified miR-205-5p-ANGPT2-AKT/ERK axis illustrates the molecular mechanism of endometriosis progression and may represent a novel diagnostic biomarker and therapeutic target for disease treatment.
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.