ArticleCell cycle (Georgetown, Tex.)2013
microRNA-141 regulates BMI1 expression and induces senescence in human diploid fibroblasts.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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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Who cites it
27 citing papers in PubMed, 49 citations in OpenAlex.
- Integrating bulk and single-cell transcriptomics to elucidate the role and potential mechanisms of autophagy in aging tissue.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- miR-23b-3p, miR-124-3p and miR-218-5p Synergistic or Additive Effects on Cellular Processes That Modulate Cervical Cancer Progression? A Molecular Balance That Needs Attention.International journal of molecular sciences · 2022Review
- Parvovirus B19 induces cellular senescence in human dermal fibroblasts: putative role in systemic sclerosis-associated fibrosis.Rheumatology (Oxford, England) · 2022Article
- MicroRNAs, Long Non-Coding RNAs, and Circular RNAs in the Redox Control of Cell Senescence.Antioxidants (Basel, Switzerland) · 2022Review
- Regulation of gene transcription of B lymphoma Mo-MLV insertion region 1 homolog (Review).Biomedical reports · 2021Review
- Maternal diabetes induces senescence and neural tube defects sensitive to the senomorphic rapamycin.Science advances · 2021Article
- MicroRNA regulation of cancer stem cells in the pathogenesis of breast cancer.Cancer cell international · 2021Review
- Review
- ZNRD1-AS1 knockdown alleviates malignant phenotype of retinoblastoma through miR-128-3p/BMI1 axis.American journal of translational research · 2021Article
- Internal Ribosome Entry Sites Mediate Cap-Independent Translation of Bmi1 in Nasopharyngeal Carcinoma.Frontiers in oncology · 2020Article
- Role of MicroRNA-141 in the Aging Musculoskeletal System: A Current Overview.Mechanisms of ageing and development · 2019Review
- Identification of Novel Genes in Osteoarthritic Fibroblast-Like Synoviocytes Using Next-Generation Sequencing and Bioinformatics Approaches.International journal of medical sciences · 2019Article
- Review
- MicroRNA 141 represses nasopharyngeal carcinoma growth through inhibiting BMI1.Oncology letters · 2018Article
- MicroRNA controls of cellular senescence.BMB reports · 2018Article
- Timosaponin A-III inhibits oncogenic phenotype via regulation of PcG protein BMI1 in breast cancer cells.Molecular carcinogenesis · 2018Article
- miR-200a Modulates the Expression of the DNA Repair Protein OGG1 Playing a Role in Aging of Primary Human Keratinocytes.Oxidative medicine and cellular longevity · 2018Article
- Article
- Identification of miR-31-5p, miR-141-3p, miR-200c-3p, and GLT1 as human liver aging markers sensitive to donor-recipient age-mismatch in transplants.Aging cell · 2017Article
- Senescence-Associated MicroRNAs.International review of cell and molecular biology · 2017Review
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4 authors at 2 institutions in 1 country.
Funding
Abstract
Polycomb group protein BMI1 is an important regulator of senescence, aging, and cancer. On one hand, it is overexpressed in cancer cells and is required for self-renewal of stem cells. On the other hand, it is downregulated during senescence and aging. MicroRNAs have emerged as major regulators of almost every gene associated with cancer, aging, and related pathologies. At present, very little is known about the miRNAs that regulate the expression of BMI1. Here, we report that miR-141 posttranscriptionally downregulates BMI1 expression in human diploid fibroblasts (HDFs) via a miR-141 targeting sequence in the 3' untranslated region of BMI1 mRNA. We also show that overexpression of miR-141 induces premature senescence in HDFs via targeting of BMI1 in normal but not in exogenous BMI1-overexpressing HDFs. Induction of premature senescence in HDFs was accompanied by upregulation of p16INK4a, an important downstream target of BMI1 and a major regulator of senescence. Our results suggest that miR-141-based therapies could be developed to treat pathologies where BMI1 is deregulated.
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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.