ArticleJournal of molecular medicine (Berlin, Germany)2017
hsa-miR-4485 regulates mitochondrial functions and inhibits the tumorigenicity of breast cancer cells.
Article in Journal of molecular medicine (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
45 citing papers in PubMed, 74 citations in OpenAlex.
- Gene Therapy Tools for Diseases Caused by Mutations of the Mitochondrial Genome.International journal of molecular sciences · 2026Review
- Prediction of lymphocyte-predominant breast cancer using microRNA expression in cytology specimens.Cancer cytopathology · 2026Article
- Decoding noncoding RNAs in regulating cardiovascular aging and age-related conditions: the emerging landscape.Science China. Life sciences · 2026Review
- The effects of SARS-CoV-2 on bone homeostasis.Frontiers in endocrinology · 2026Review
- Exercise-responsive microRNA networks and extracellular vesicle-mediated microRNA signaling in breast cancer: linking tumor signaling, systemic crosstalk, and clinical relevance.Frontiers in oncology · 2026Review
- Article
- Regulating the expression of exercise-induced micro-RNAs and long non-coding RNAs: implications for controlling cardiovascular diseases and heart failure.Frontiers in molecular biosciences · 2025Review
- Mitochondrial epigenetic mechanisms in cancer: an updated overview.Frontiers in cell and developmental biology · 2025Review
- Combinatorial phenethyl isothiocyanate and withaferin A targets multiple epigenetics pathways to inhibit MCF-7 and MDA-MB-231 human breast cancer cells.Cancer cell international · 2024Article
- Tailored apoptotic vesicles promote bone regeneration by releasing the osteoinductive brake.International journal of oral science · 2024Article
- Global miRNA profiling reveals key molecules that contribute to different chronic lymphocytic leukemia incidences in Asian and Western populations.Haematologica · 2024Article
- Extracellular vesicles secreted by 3D tumor organoids are enriched for immune regulatory signaling biomolecules compared to conventional 2D glioblastoma cell systems.Frontiers in immunology · 2024Article
- Roles of MT-ND1 in Cancer.Current medical science · 2023Review
- Exploring the Therapeutic Potential ofInternational journal of molecular sciences · 2023Article
- MiRNAs Action and Impact on Mitochondria Function, Metabolic Reprogramming and Chemoresistance of Cancer Cells: A Systematic Review.Biomedicines · 2023Review
- Mitochondrial-related microRNAs and their roles in cellular senescence.Frontiers in physiology · 2023Review
- Primary oxidative phosphorylation defects lead to perturbations in the human B cell repertoire.Frontiers in immunology · 2023Article
- Challenging Cellular Homeostasis: Spatial and Temporal Regulation of miRNAs.International journal of molecular sciences · 2022Review
- Non-canonical features of microRNAs: paradigms emerging from cardiovascular disease.Nature reviews. Cardiology · 2022Review
- Transcriptome Profiling of ADAR1 Targets in Triple-Negative Breast Cancer Cells Reveals Mechanisms for Regulating Growth and Invasion.Molecular cancer research : MCR · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The modulation of mitochondrial functions is important for maintaining cellular homeostasis. Mitochondria essentially depend on the import of RNAs and proteins encoded by the nuclear genome. MicroRNAs encoded in the nucleus can translocate to mitochondria and target the genome, affecting mitochondrial function. Here, we analyzed the role of miR-4485 in the regulation of mitochondrial functions. We showed that miR-4485 translocated to mitochondria where its levels varied in response to different stress conditions. A direct binding of miR-4485 to mitochondrial 16S rRNA was demonstrated. MiR-4485 regulated the processing of pre-rRNA at the 16S rRNA-ND1 junction and the translation of downstream transcripts. MiR-4485 modulated mitochondrial complex I activity, the production of ATP, ROS levels, caspase-3/7 activation, and apoptosis. Transfection of a miR-4485 mimic downregulated the expression of regulatory glycolytic pathway genes and reduced the clonogenic ability of breast cancer cells. Ectopic expression of miR-4485 in MDA-MB-231 breast carcinoma cells decreased the tumorigenicity in a nude mouse xenograft model. Furthermore, levels of both precursor and mature miR-4485 are decreased in tumor tissue of breast cancer patients. We conclude that the mitochondria-targeted miR-4485 may act as a tumor suppressor in breast carcinoma cells by negatively regulating mitochondrial RNA processing and mitochondrial functions.
Indexed as
Identifiers
What OpenQuestion holds
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.