ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2013
Regulation of human RNase-L by the miR-29 family reveals a novel oncogenic role in chronic myelogenous leukemia.
Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- The miRNA Landscape of Leukemia - Cellular Actions to Therapy through Molecular Mechanisms.Cell biochemistry and biophysics · 2025Review
- Endonucleolytic RNA cleavage drives changes in gene expression during the innate immune response.Cell reports · 2024Article
- Activation of the antiviral factor RNase L triggers translation of non-coding mRNA sequences.Nucleic acids research · 2021Article
- MicroRNA-29 family inhibits rhabdomyosarcoma formation and progression by regulating GEFT function.American journal of translational research · 2020Article
- Review
- Zebrafish microRNA miR-210-5p inhibits primitive myelopoiesis by silencingThe Journal of biological chemistry · 2019Article
- MicroRNAs mediated regulation of MAPK signaling pathways in chronic myeloid leukemia.Oncotarget · 2016Review
- The Role of MicroRNAs in Myeloproliferative Neoplasia.International journal of hematology-oncology and stem cell research · 2016Review
- Oncogenic kinase fusions: an evolving arena with innovative clinical opportunities.Oncotarget · 2016Review
- The Roles of RNase-L in Antimicrobial Immunity and the Cytoskeleton-Associated Innate Response.International journal of molecular sciences · 2016Review
- Potential roles of microRNA-29a in the molecular pathophysiology of T-cell acute lymphoblastic leukemia.Cancer science · 2015Article
- miR-29s: a family of epi-miRNAs with therapeutic implications in hematologic malignancies.Oncotarget · 2015Review
- Metformin inhibits tumor growth by regulating multiple miRNAs in human cholangiocarcinoma.Oncotarget · 2015Article
- RNase-L control of cellular mRNAs: roles in biologic functions and mechanisms of substrate targeting.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Review
- Altered expression pattern of miR-29a, miR-29b and the target genes in myeloid leukemia.Experimental hematology & oncology · 2014Article
- Can't RIDD off viruses.Frontiers in microbiology · 2014Review
- RNASEL and MIR146A SNP-SNP interaction as a susceptibility factor for non-melanoma skin cancer.PloS one · 2014Article
- Reciprocal inhibition between intracellular antiviral signaling and the RNAi machinery in mammalian cells.Cell host & microbe · 2013Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The endoribonuclease RNase-L is the terminal component of an interferon-regulated RNA decay pathway known as the 2'-5'-oligoadenylate (2-5A) system, whose established functions include antimicrobial and tumor suppressive activities. RNase-L activity requires binding of the small molecule 2-5A, leading to RNase-L dimerization and cleavage of single-stranded RNA. RNase-L expression is controlled post-transcriptionally by its 3'-untranslated region (3' UTR), which exerts a strong negative effect on RNase-L levels. MicroRNAs (miRNAs) are a class of small noncoding RNAs that repress expression of target genes by binding to regions of complementarity often in the 3' UTR. The miR-29 family acts as a tumor suppressor in several cancers, including acute and chronic myelogenous leukemia (CML), and has many oncogenic targets. We report that the miR-29 family represses RNase-L protein expression across several cell types. Using a luciferase reporter, we showed that miR-29 acts via 4 target sites within the RNASEL 3' UTR. Mutation of all sites is required for abrogation of miR-29 repression. In light of the reported tumor suppressive role of miR-29 in K562 CML cells and miR-29 repression of RNase-L in these cells, we generated K562 cells with stable RNase-L knockdown and demonstrated that loss of RNase-L inhibits proliferation in vitro as well as tumor growth in a xenograft model. Our findings identify a previously unknown miRNA regulator of RNase-L expression and support a novel oncogenic role for RNase-L in CML and potentially other hematopoietic malignancies.
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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.