ArticlePloS one2014
Mir-34a mimics are potential therapeutic agents for p53-mutated and chemo-resistant brain tumour cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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
22 citing papers in PubMed, 39 citations in OpenAlex.
- Engineered smart materials for RNA based molecular therapy to treat Glioblastoma.Bioactive materials · 2024Article
- Glioblastoma Therapy: Past, Present and Future.International journal of molecular sciences · 2024Review
- Engineering HEK293T cell line by lentivirus to produce miR34a-loaded exosomes.Molecular biology reports · 2023Article
- Exploring the Role of microRNAs in Glioma Progression, Prognosis, and Therapeutic Strategies.Cancers · 2023Review
- microRNAs (miRNAs) in Glioblastoma Multiforme (GBM)-Recent Literature Review.International journal of molecular sciences · 2023Review
- Role of MicroRNAs in the Development and Progression of the Four Medulloblastoma Subgroups.Cancers · 2021Review
- Noncoding RNAs in pediatric brain tumors: Molecular functions and pathological implications.Molecular therapy. Nucleic acids · 2021Review
- Article
- Role of microRNAs in glioblastoma.Oncotarget · 2021Article
- Anesthetics may modulate cancer surgical outcome: a possible role of miRNAs regulation.BMC anesthesiology · 2021Review
- Falcarindiol and dichloromethane fraction are bioactive components inJournal of applied biomedicine · 2021Article
- SIRT1 and AROS suppress doxorubicin-induced apoptosis via inhibition of GSK3β activity in neuroblastoma cells.Animal cells and systems · 2020Article
- The Non-coding Side of Medulloblastoma.Frontiers in cell and developmental biology · 2020Review
- MiR-34a overexpression enhances the inhibitory effect of doxorubicin on HepG2 cells.World journal of gastroenterology · 2019Article
- Decrease of Nibrin expression in chronic hypoxia is associated with hypoxia-induced chemoresistance in some brain tumour cells.BMC cancer · 2019Article
- MiR-21, miR-34a, miR-125b, miR-181d and miR-648 levels inversely correlate with MGMT and TP53 expression in primary glioblastoma patients.Archives of medical science : AMS · 2019Article
- Molecular pathways involved in microRNA-mediated regulation of multidrug resistance.Molecular biology reports · 2018Review
- miR miR on the wall, who's the most malignant medulloblastoma miR of them all?Neuro-oncology · 2018Review
- Regulation of multidrug resistance by microRNAs in anti-cancer therapy.Acta pharmaceutica Sinica. B · 2017Review
- MicroRNAs in glioblastoma multiforme pathogenesis and therapeutics.Cancer medicine · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Chemotherapeutic drug resistance and relapse remains a major challenge for paediatric (medulloblastoma) and adult (glioblastoma) brain tumour treatment. Medulloblastoma tumours and cell lines with mutations in the p53 signalling pathway have been shown to be specifically insensitive to DNA damaging agents. The aim of this study was to investigate the potential of triggering cell death in p53 mutated medulloblastoma cells by a direct activation of pro-death signalling downstream of p53 activation. Since non-coding microRNAs (miRNAs) have the ability to fine tune the expression of a variety of target genes, orchestrating multiple downstream effects, we hypothesised that triggering the expression of a p53 target miRNA could induce cell death in chemo-resistant cells. Treatment with etoposide, increased miR-34a levels in a p53-dependent fashion and the level of miR-34a transcription was correlated with the cell sensitivity to etoposide. miR-34a activity was validated by measuring the expression levels of one of its well described target: the NADH dependent sirtuin1 (SIRT1). Whilst drugs directly targeting SIRT1, were potent to trigger cell death at high concentrations only, introduction of synthetic miR-34a mimics was able to induce cell death in p53 mutated medulloblastoma and glioblastoma cell lines. Our results show that the need of a functional p53 signaling pathway can be bypassed by direct activation of miR-34a in brain tumour cells.
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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.