ArticleGenes2018
MicroRNA-106a-5p Inhibited C2C12 Myogenesis via Targeting PIK3R1 and Modulating the PI3K/AKT Signaling.
Article in Genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.
- A Systematic Review and User Reference of Phenotypic and Molecular Characteristics of Dexamethasone-Mediated C2C12 Muscle Atrophy.Journal of cachexia, sarcopenia and muscle · 2026Pooled it
- MicroRNAs in obesity, sarcopenia, and commonalities for sarcopenic obesity: a systematic review.Journal of cachexia, sarcopenia and muscle · 2022Pooled it
- Review
- Article
- Review
- Transcriptome sequencing and bioinformatics analysis of gastrocnemius muscle in type 2 diabetes mellitus rats.BMC musculoskeletal disorders · 2024Article
- Review
- Article
- Ursolic acid improves the indoxyl sulfate-induced impairment of mitochondrial biogenesis in C2C12 cells.Nutrition research and practice · 2022Article
- Article
- Article
- Expression levels of specific microRNAs are increased after exercise and are associated with cognitive improvement in Parkinson's disease.Molecular medicine reports · 2021Article
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- Article
- MicroRNA regulatory networks in the pathogenesis of sarcopenia.Journal of cellular and molecular medicine · 2020Review
- The regulatory role of Myomaker and Myomixer-Myomerger-Minion in muscle development and regeneration.Cellular and molecular life sciences : CMLS · 2020Review
- Long Non-coding RNAFrontiers in cell and developmental biology · 2020Article
- miR-106a-5p Functions as a Tumor Suppressor by Targeting VEGFA in Renal Cell Carcinoma.Disease markers · 2020Article
- Silencing of miR-17-5p suppresses cell proliferation and promotes cell apoptosis by directly targeting PIK3R1 in laryngeal squamous cell carcinoma.Cancer cell international · 2020Article
- 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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The microRNA (miR)-17 family is widely expressed in mammalian tissues and play important roles in various physiological and pathological processes. Here, the functions of miR-106a-5p, a member of miR-17 family, were explored during myogenic differentiation in C2C12 cell line. First, miR-106a-5p was found to be relatively lower expressed in two-month skeletal muscle tissues and gradually decreased upon myogenic stimuli. Forced expression of miR-106a-5p significantly reduced the differentiation index, fusion index as well as the expression of myogenic markers (MyoD, MyoG, MyHC, Myomixer, Myomarker). Meanwhile, the levels of phosphorylated AKT were reduced by overexpression of miR-106a-5p, and administration of insulin-like growth factor 1 (IGF1), a booster of myogenic differentiation, could recover all the inhibitory effects above of miR-106a-5p. Furthermore, miR-106a-5p was elevated in aged muscles and dexamethasone (DEX)-treated myotubes, and up-regulation of miR-106a-5p significantly reduced the diameters of myotubes accompanied with increased levels of muscular atrophy genes and decreased PI3K/AKT activities. Finally, miR-106a-5p was demonstrated to directly bind to the 3'-UTR of PIK3R1, thus, repress the PI3K/AKT signaling.
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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.