ArticleOncotarget2017
Involment of RAS/ERK1/2 signaling and MEF2C in miR-155-3p inhibition-triggered cardiomyocyte differentiation of embryonic stem cell.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Human Hematopoietic Stem Cells Enhance Maturational Differentiation of hiPSC-Derived Cardiomyocytes on Xeno-Free MatriClone-Plastic via EGFR/MAPK/ERK Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2026Article
- The regulation of miR-155 strand selection by CELF2, FUBP1 and KSRP proteins.Scientific reports · 2025Article
- Proteomic Investigation of Neurotrophic trans-Banglene Reveals Potential Link to Iron Homeostasis.Molecular neurobiology · 2025Article
- Epigenetic Modification Factors and microRNAs Network Associated with Differentiation of Embryonic Stem Cells and Induced Pluripotent Stem Cells toward Cardiomyocytes: A Review.Life (Basel, Switzerland) · 2023Review
- miR-155-3p: processing by-product or rising star in immunity and cancer?Open biology · 2022Review
- MicroRNAs and Stem-like Properties: The Complex Regulation Underlying Stemness Maintenance and Cancer Development.Biomolecules · 2021Review
- Therapeutic Approaches for Metastases from Colorectal Cancer and Pancreatic Ductal Carcinoma.Pharmaceutics · 2021Review
- AMPKβ1 and AMPKβ2 define an isoform-specific gene signature in human pluripotent stem cells, differentially mediating cardiac lineage specification.The Journal of biological chemistry · 2020Article
- MiR-206-3p alleviates chronic constriction injury-induced neuropathic pain through targeting HDAC4.Experimental animals · 2019Article
- The MicroRNA-551a/MEF2C Axis Regulates the Survival and Sphere Formation of Cancer Cells in Response to 5-Fluorouracil.Molecules and cells · 2019Article
- Transient up-regulation of miR-155-3p by lipopolysaccharide in primary human monocyte-derived macrophages results in RISC incorporation but does not alter TNF expression.Wellcome open research · 2019Article
- A MicroRNA Perspective on Cardiovascular Development and Diseases: An Update.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) are short, noncoding RNAs that regulate post-transcriptional gene expression by targeting messenger RNAs (mRNAs) for cleavage or translational repression. Growing evidence indicates that miR-155 expression changes with the development of heart and plays an important role in heart physiopathology. However, the role of miR-155 in cardiac cells differentiation is unclear. Using the well-established embryonic stem cell (ESC), we demonstrated that miR-155-3p expression was down-regulated during cardiogenesis from mouse ESC. By contrast, the myogenic enhance factor 2C (MEF2C), a predicted target gene of miR-155-3p, was up-regulated. We further demonstrated that miR-155-3p inhibition increased the percentage of embryoid bodies (EB) beating and up-regulated the expression of cardiac specific markers, GATA4, Nkx2.5, and cTnT mRNA and protein. Notably, miR-155-3p inhibition caused upregulation of MEF2C, KRAS and ERK1/2. ERK1/2 inhibitor, PD98059 significantly decreased the expression of MEF2C protein. These findings indicate that miR-155-3p inhibition promotes cardiogenesis, and its mechanisms are involved in the RAS-ERK1/2 signaling and MEF2C.
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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.