ArticleCell structure and function2019
MiR-187-3p Enhances Propranolol Sensitivity of Hemangioma Stem Cells.
Article in Cell structure and function, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- lncRNA NEAT1 promotes the proliferation of hemangioma cells by transcriptionally activating β‑catenin via enhancing H3K18 lactylation.Molecular medicine reports · 2026Article
- The emerging role of non-coding RNAs in the pathogenesis of infantile hemangioma.Cancer cell international · 2025Review
- MiR-27b-3p Reduces the Efficacy of Propranolol in the Treatment of Infantile Hemangioma by Inhibiting the Expression of Apaf-1.Biomedicines · 2025Article
- Non-coding RNA in infantile hemangioma.Pediatric research · 2024Review
- ALKBH5 facilitates the progression of infantile hemangioma by increasing FOXF1 expression in a mMolecular and cellular biochemistry · 2024Article
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- MicroRNA-195-5p inhibits the progression of hemangioma via targeting SKI.Experimental and therapeutic medicine · 2022Article
- The Cohesin Complex and Its Interplay with Non-Coding RNAs.Non-coding RNA · 2021Review
- Propranolol inhibits infantile hemangioma by regulating the miR-424/vascular endothelial growth factor-A (VEGFA) axis.Translational pediatrics · 2021Article
- Long non-coding RNA TUG1/microRNA-187-3p/TESC axis modulates progression of pituitary adenoma via regulating the NF-κB signaling pathway.Cell death & disease · 2021Article
- MiR-206 promotes extracellular matrix accumulation and relieves infantile hemangioma through targeted inhibition of DNMT3A.Cell cycle (Georgetown, Tex.) · 2021Article
- Exosome-derived miR-196b-5p facilitates intercellular interaction in infantile hemangioma via down-regulating CDKN1B.Annals of translational medicine · 2021Article
- BETting on a Transcriptional Deficit as the Main Cause for Cornelia de Lange Syndrome.Frontiers in molecular biosciences · 2021Review
- IADVL SIG Pediatric Dermatology (Academy) Recommendations on Hemangioma of Infancy (HOI).Indian dermatology online journalReview
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infantile hemangioma is the most common soft tissue tumors in childhood. In clinic, propranolol is widely used for infantile hemangioma therapy. However, some of the infantile hemangioma patients display resistance to propranolol treatment. Previous studies show that miR-187-3p is inhibited in hepatocellular carcinoma and lung cancer, while the role of miR-187-3p in infantile hemangioma remains unclear. In the present study, we explore the biological role of miR-187-3p in infantile hemangioma. The mRNA and protein levels of related genes were detected by real-time PCR and Western blotting. CCK8 assay was used to detect cell viability and IC50 values of propranolol. Cell apoptosis was detected by Caspase-3 Activity assay. Luciferase reporter assay and biotin RNA pull down assay were used to detect the interaction between miR-187-3p and the targeted gene. MiR-187-3p was down-regulated in infantile hemangioma tissues and promoted propranolol sensitivity of HemSCs. Mechanically, NIPBL was the direct target of miR-187-3p in HemSCs. NIPBL downregulation inhibited propranolol resistance of HemSCs. Re-introduction of NIPBL reversed miR-187-3p-meidated higher propranolol sensitivity of HemSCs. MiR-187-3p enhanced propranolol sensitivity of hemangioma stem cells via targeting NIPBL. MiR-187-3p may serve as a novel prognostic indicator and potential target for infantile hemangioma therapy.Key words: MiR-187-3p, infantile hemangioma, propranolol, resistance, NIPBL.
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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.