ArticleBMC cancer2019
miR-520d-5p can reduce the mutations in hepatoma cancer cells and iPSCs-derivatives.
Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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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
4 citing papers in PubMed, 9 citations in OpenAlex.
- Placenta-derived small extracellular vesicles transfer miR-520d-5p to mediate pancreatic β-cell injury in gestational diabetes mellitus by targeting SIRT1.BMC pregnancy and childbirth · 2026Article
- Unraveling the anti-tumor effects of midazolam in non-small cell lung cancer through the lncRNA XLOC_010706/miR-520d-5p/STAT3/autophagy pathway.Scientific reports · 2025Article
- Article
- Circular RNA FNDC3B Protects Oral Squamous Cell Carcinoma Cells From Ferroptosis and Contributes to the Malignant Progression by Regulating miR-520d-5p/SLC7A11 Axis.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundHuman microRNAs (miRNAs) have diverse functions in biology, and play a role in nearly every biological process. Here we report that miR-520d-5p (520d-5p) causes undifferentiated cancer cells to adopt benign or normal status in vivo in immunodeficient mice via demethylation and P53 upregulation. Further we found that 520-5p causes normal cells to elongate cellular lifetime and mesenchymal stem cell-like status with CD105 positivity. We hypothesized that ectopic 520d-5p expression reduced mutations in undifferentiated type of hepatoma (HLF) cells through synergistic modulation of methylation-related enzymatic expression.
methodsTo examine whether there were any changes in mutation status in cells treated with 520d-5p, we performed next generation sequencing (NGS) in HLF cells and human iPSC-derivative cells in pre-mesenchymal stem cell status. We analyzed the data using both genome-wide and individual gene function approaches.
results520d-5p induced a shift towards a wild type or non-malignant phenotype, which was regulated by nucleotide mutations in both HLF cells and iPSCs. Further, 520d-5p reduced mutation levels in both the whole genome and genomic fragment assemblies.
conclusionsCancer cell genomic mutations cannot be repaired in most contexts. However, these findings suggest that applied development of 520d-5p would allow new approaches to cancer research and improve the quality of iPSCs used in regenerative medicine.
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Registered trials
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