ArticleNucleic acids research2013
A Myc-microRNA network promotes exit from quiescence by suppressing the interferon response and cell-cycle arrest genes.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 50 citations in OpenAlex.
- The emerging role of microRNA-22 in the Leukemia: experimental and clinical implications.Molecular biology reports · 2023Review
- HECTD3 promotes gastric cancer progression by mediating the polyubiquitination of c-MYC.Cell death discovery · 2022Article
- Circulating microRNA signatures associated with disease severity and outcome in COVID-19 patients.Frontiers in immunology · 2022Article
- A Combined mRNA- and miRNA-Sequencing Approach Reveals miRNAs as Potential Regulators of the Small Intestinal Transcriptome in Celiac Disease.International journal of molecular sciences · 2021Article
- Virus-Induced Tumorigenesis and IFN System.Biology · 2021Review
- Antagonism between splicing and microprocessor complex dictates the serum-induced processing of lnc-RNA (New York, N.Y.) · 2020Article
- Genetic Programs Driving Oncogenic Transformation: Lessons from in Vitro Models.International journal of molecular sciences · 2019Article
- TRIP13 promotes the cell proliferation, migration and invasion of glioblastoma through the FBXW7/c-MYC axis.British journal of cancer · 2019Article
- MicroRNAs reinforce repression of PRC2 transcriptional targets independently and through a feed-forward regulatory network.Genome research · 2019Article
- Circular RNA CircEZH2 Suppresses Transmissible Gastroenteritis Coronavirus-induced Opening of Mitochondrial Permeability Transition Pore via Targeting MiR-22 in IPEC-J2.International journal of biological sciences · 2019Article
- Review
- MicroRNA Microarray Profiling during Megakaryocyte Differentiation of Cord Blood CD133+ Hematopoietic Stem Cells.Cell journal · 2018Article
- Transcription factor FoxM1 is the downstream target of c-Myc and contributes to the development of prostate cancer.World journal of surgical oncology · 2018Article
- An In Vitro Model of Cellular Quiescence in Primary Human Dermal Fibroblasts.Methods in molecular biology (Clifton, N.J.) · 2018Article
- MicroRNA-22 controls interferon alpha production and erythroid maturation in response to infectious stress in mice.Experimental hematology · 2017Article
- Widespread changes in mRNA stability contribute to quiescence-specific gene expression patterns in a fibroblast model of quiescence.BMC genomics · 2017Article
- MiR-200c is a cMyc-activated miRNA that promotes nasopharyngeal carcinoma by downregulating PTEN.Oncotarget · 2017Article
- Plasma miR-22-3p, miR-642b-3p and miR-885-5p as diagnostic biomarkers for pancreatic cancer.Journal of cancer research and clinical oncology · 2017Article
- c-MYC drives histone demethylase PHF8 during neuroendocrine differentiation and in castration-resistant prostate cancer.Oncotarget · 2016Article
- Systematic integration of molecular profiles identifies miR-22 as a regulator of lipid and folate metabolism in breast cancer cells.Oncogene · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The transition of mammalian cells from quiescence to proliferation is accompanied by the differential expression of several microRNAs (miRNAs) and transcription factors. However, the interplay between transcription factors and miRNAs in modulating gene regulatory networks involved in human cell proliferation is largely unknown. Here we show that the miRNA miR-22 promotes proliferation in primary human cells, and through a combination of Argonaute-2 immunoprecipitation and reporter assays, we identified multiple novel targets of miR-22, including several cell-cycle arrest genes that mediate the effects of the tumor-suppressor p53. In addition, we found that miR-22 suppresses interferon gene expression by directly targeting high mobility group box-1 and interferon regulatory factor (IRF)-5, preventing activation of IRF3 and NF-κB, which are activators of interferon genes. The expression of interferon genes is elevated in quiescent cells and their expression is inhibitory for cell proliferation. In addition, we find that miR-22 is activated by the transcription factor Myc when quiescent cells enter proliferation and that miR-22 inhibits the Myc transcriptional repressor MXD4, mediating a feed-forward loop to elevate Myc expression levels. Our results implicate miR-22 in downregulating the anti-proliferative p53 and interferon pathways and reveal a new transcription factor-miRNA network that regulates the transition of primary human cells from quiescence to proliferation.
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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.